Profit of Doom
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I think there’s some problem with this approach.
CORONA Main Coronavirus thread
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Heliobas Disciple
TB Fanatic
I don't always agree with the articles I post, I try to post what I find without personal opinion entering into it since this is an archive thread of the articles out there about covid. I agree with your comment, I think that the vaccinated may push variants, not the unvaccinated because of antibody dependent enhancement as was discussed way back on this thread especially by Geert Vanden Bossche among others.
HD
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Heliobas Disciple
TB Fanatic
Ivermectin in Florida and Brazil
19min 21sec
Mar 6, 2022
Dr. John Campbell
Follow the evidence, wherever it leads Treatment with Ivermectin Is Associated with Decreased Mortality in COVID-19 Patients: Analysis of a National Federated Database https://bnf.nice.org.uk/medicinal-for... https://list.essentialmeds.org https://www.sciencedirect.com/science... https://www.sciencedirect.com/science... https://www.sciencedirect.com/journal... Purpose To evaluate the difference in mortality, Patients treated with ivermectin Patients treated with remdesivir 44 healthcare organizations and 68 million patients from US, January 1, 2020 and July 11, 2021 Methods & Materials Retrospectively identified diagnosed adults Recorded use of ivermectin, but not remdesivir Recorded use of remdesivir, but not ivermectin Controlled for, comorbidities, and treatments that may affect COVID-19 survival outcomes: age, gender, race, ethnicity, nicotine use diabetes mellitus, obesity, chronic lower respiratory disease, ischemic heart diseases, tocilizumab, glucocorticoids, or ventilator use. Primary outcome assessed, mortality Sith significance assessed at p less than 0.05. Result 41,608 patients who had COVID-19 Treated with ivermectin n = 1,072 Treated with remdesivir n = 40,536 Ivermectin was associated with reduced mortality vs remdesivir OR 0.308 p less than 0.0001. Conclusion Ivermectin use was associated with decreased mortality in patients with COVID-19 compared to remdesivir. In the future, if more publications are published with the similar result to the current analyses, the certainty of evidence will increase. Ivermectin Prophylaxis Used for COVID-19: A Citywide, Prospective, Observational Study of 223,128 Subjects Using Propensity Score Matching (Brazil) https://www.cureus.com/articles/82162... Background Ivermectin has demonstrated different mechanisms of action, coronavirus infection and COVID-19-related comorbidities. Prophylaxis combined with the known safety profile of ivermectin Study to evaluate the impact of regular ivermectin use on subsequent COVID-19 infection and mortality rates. Prospective, July 2020 and December 2020 Inviting the entire population of Itajaí to a medical visit to enroll in the program, ivermectin was offered as an optional treatment to be taken for two consecutive days every 15 days at a dose of 0.2 mg/kg/day. Study analysis consisted of comparing ivermectin users with non-users using cohorts Results 223,128 citizens of Itajaí considered 159,561 included in the analysis 113,845 (71.3%) regular ivermectin users 45,716 (23.3%) non-users Of these 4,311 ivermectin users were infected, (3.7% infection rate) 3,034 non-users (6.6% infection rate) A 44% reduction in COVID-19 infection rate Risk ratio (RR), 0.56 The regular use of ivermectin led to a 68% reduction in COVID-19 mortality Deaths 25 (0.8%) deaths in the ivermectin group 79 (2.6%) among ivermectin non-users RR, 0.32 p less than 0.0001 When adjusted for residual variables, reduction in mortality rate was 70% There was a 56% reduction in hospitalization rate 44 in the ivermectin group 99 in non ivermectin users After adjustment for residual variables, reduction in hospitalization rate was 67% p less than 0.0001 Conclusion In this large study, regular use of ivermectin as a prophylactic agent was associated with significantly reduced COVID-19 infection, hospitalization, and mortality rates.
Heliobas Disciple
TB Fanatic
China Mandates COVID-Zero Policy in Shenzhen; Locals Struggle to Source Food
www.theepochtimes.com
China Mandates COVID-Zero Policy in Shenzhen; Locals Struggle to Source Food
By Nicole Hao
March 5, 2022 Updated: March 6, 2022
The Chinese regime continues to mandate its COVID-zero policy that quarantines all potential infections and locks down cities.
Residents in Shenzhen, a city with multiple districts reporting outbreaks of COVID-19, complained that they were surrounded by “trash mountains” and in desperate need of food due to the lockdown.
“On the evening of Feb. 28, a neighbor tried to jump off the building from his apartment. Other neighbors told me that he has depression and hadn’t eaten for two days. He lost all hope and tried to commit suicide,” Lin Dai (pseudonym), a resident of Shangshadong village in the city of Shenzhen, told the Chinese-language Epoch Times on March 2.
“After we were locked down at home, we couldn’t go out to buy food. I tried to order online, but it was very difficult to find food that can be delivered to us,” Lin said.
“I know a young woman who lives in my building. She only has rice and pickles at home. She tries to eat as little as possible, and has eaten only one or two bowls of congee with pickles every day in the past days.”
“We continually called the authorities for help and were told they don’t have enough manpower to take care of the residents who are under lockdown,” Lin said. “Finally, the regime sent us milk and apples this morning and some fast food and vegetables at noon.”
Chen Dong (pseudonym) is a new Shenzhen resident who drives a taxi in the city. On Feb. 22, Chen was locked down at his apartment in Shangshadong village. Since then, he hasn’t been able to work and can’t earn any money.
“The regime said that their staff members would send food to our doors, but the majority of the volunteers who bring the food don’t dare to come here. They are afraid of being infected,” Chen said. “In the first days, we could go downstairs to pick up the food from the building’s front door.”
The lives of Chen and his neighbors became worse on Feb 26, when the regime suddenly wouldn’t allow them to leave their apartments.
“They locked our building, didn’t send us anything, and didn’t remove the trash. Now, the trash is everywhere and piled like mountains,” Chen said. “Nobody takes care of us, and many people shouted from their windows that they were hungry and needed food.”
On March 1, Chen and his neighbors received the first batch of food, which Chen didn’t think was sufficient for a family.
“We have no other solution. If a family hasn’t stocked up food, and there are children, they will die of hunger. We went upstairs and downstairs to check on our neighbors. We are helping each other,” Chen said.
Li Fei (pseudonym), a regime clerk at Shatou community in Shenzhen, told the Chinese-language Epoch Times on March 2 that the regime sealed the residential buildings and compounds where new infections were reported using barbed wire. “We don’t allow any resident to escape from the sealed area.”
Li said that about 60,000 to 70,000 people live at Shangsha village in the community and all are locked in their homes.
Mass Testing
Like other Chinese cities, the Shenzhen authorities mandated that all residents in the city must have a COVID-19 test every three days. On March 2, the regime announced that people aren’t allowed to take the metro if they don’t have a negative COVID-19 test result within 48 hours.
Inside residential compounds, speakers continually broadcast: “Your health code will turn to yellow if you haven’t been tested in the past 72 hours” and “You can’t go to work tomorrow if you don’t take a test today.”
A resident surnamed Chen who lives at Shekou community in Nanshan district in Shenzhen said in a phone interview that she and the majority of Shenzhen residents work to earn money. “The rule that people can’t work without a test, strangles our throats. It’ll be horrible if a Shenzhen resident can’t go to work,” Ms. Chen said.
The Chinese regime doesn’t allow people to move without a cell phone app-generated health code. A green code means the owner can pass the checkpoints for public transportation, enter a building, or even go back home. A yellow code means the owner has to stay at home. A red code means the owner must be quarantined at a quarantine center.
The nucleic acid tests in China are linked to each resident’s health code app. If the app hasn’t received a required test result, the code will show yellow. The system forces Chinese people to take the test.
However, the mass testing was believed to be a breeding ground for COVID-19.
“On Feb. 22, the community clerks ordered us to take the nucleic acid test for COVID-19. We were crowded together and had to wait for over four hours,” Chen Dong said. “We are required to be tested even now.”
On March 3, the Shenzhen city regime announced at the daily press conference that new infections were reported in Futian, Luohu, Nanshan, Bao’an, and Yantian districts.
On Thursday, China’s national health commission announced new domestic infections were reported in Guangdong, Inner Mongolia, Hubei, Jilin, Shanghai, Guangxi, Tianjin, Hebei, Shanxi, Heilongjiang, Jiangsu, Sichuan, and Yunnan provinces.
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Heliobas Disciple
TB Fanatic
Death toll nears 6 million as pandemic enters its 3rd year
The official global death toll from COVID-19 is on the verge of eclipsing 6 million—underscoring that the pandemic, now entering its third year, is far from over.
Death toll nears 6 million as pandemic enters its 3rd year
by David Rising
March 6, 2022
The official global death toll from COVID-19 is on the verge of eclipsing 6 million—underscoring that the pandemic, now in its third year, is far from over.
The milestone is the latest tragic reminder of the unrelenting nature of the pandemic even as people are shedding masks, travel is resuming and businesses are reopening around the globe. The death toll, compiled by Johns Hopkins University, stood at 5,996,882 as of Sunday morning and was expected to pass the 6 million mark later in the day.
Remote Pacific islands, whose isolation had protected them for more than two years, are just now grappling with their first outbreaks and deaths, fueled by the highly contagious omicron variant.
Hong Kong, which is seeing deaths soar, is testing its entire population of 7.5 million three times this month as it clings to mainland China's "zero-COVID" strategy.
As death rates remain high in Poland, Hungary, Romania and other Eastern European countries, the region has seen more than 1 million refugees arrive from war-torn Ukraine, a country with poor vaccination coverage and high rates of cases and deaths.
And despite its wealth and vaccine availability, the United States is nearing 1 million reported deaths on its own.
Death rates worldwide are still highest among people unvaccinated against the virus, said Tikki Pang, a visiting professor at the National University of Singapore's medical school and co-Chair of the Asia Pacific Immunization Coalition.
"This is a disease of the unvaccinated—look what is happening in Hong Kong right now, the health system is being overwhelmed," said Pang, the former director of research policy and cooperation with the World Health Organization. "The large majority of the deaths and the severe cases are in the unvaccinated, vulnerable segment of the population."
It took the world seven months to record its first million deaths from the virus after the pandemic began in early 2020. Four months later another million people had died, and 1 million have died every three months since, until the death toll hit 5 million at the end of October. Now it has reached 6 million—more than the populations of Berlin and Brussels combined, or the entire state of Maryland.
But despite the enormity of the figure, the world undoubtedly hit its 6 millionth death some time ago. Poor record-keeping and testing in many parts of the world has led to an undercount in coronavirus deaths, in addition to excess deaths related to the pandemic but not from actual COVID-19 infections, like people who died from preventable causes but could not receive treatment because hospitals were full.
Edouard Mathieu, head of data for the Our World in Data portal, said that—when countries' excess mortality figures are studied—as many as nearly four times the reported death toll have likely died because of the pandemic.
An analysis of excess deaths by a team at The Economist estimates that the number of COVID-19 deaths is between 14 million and 23.5 million.
"Confirmed deaths represent a fraction of the true number of deaths due to COVID, mostly because of limited testing, and challenges in the attribution of the cause of death," Mathieu told The Associated Press. "In some, mostly rich, countries that fraction is high and the official tally can be considered to be fairly accurate, but in others it is highly underestimated."
The United States has the biggest official death toll in the world, but the numbers have been trending downward over the last month.
Lonnie Bailey lost his 17-year-old nephew, Carlos Nunez Jr., who contracted COVID-19 last April—the same month Kentucky opened his age group to vaccinations. The Louisville resident said the family is still suffering, including Carlos' younger sibling, who had to be hospitalized himself and still has lingering symptoms. The aggressive reopening of the country has been jarring for them to witness.
"For us it is hard to let our guard down; it's going to take a while for us to adjust," Bailey said.
The world has seen more than 445 million confirmed COVID-19 cases, and new weekly cases have been declining recently in all regions except for the Western Pacific, which includes China, Japan and South Korea, among others, the World Health Organization reported this week.
Although the overall figures in the Pacific islands seeing their first outbreaks are small compared to larger countries, they are significant among their tiny populations and threaten to overwhelm fragile health care systems.
"Given what we know about COVID ... it's likely to hit them for the next year or so at least," said Katie Greenwood, head of the Red Cross Pacific delegation.
Tonga reported its first outbreak after the virus arrived with international aid vessels following the Jan. 15 eruption of a massive volcano, followed by a tsunami. It now has several hundred cases, but—with 66% of its population fully vaccinated—it has so far reported people suffering mostly mild symptoms and no deaths.
The Solomon Islands saw the first outbreak in January and now has thousands of cases and more than 100 deaths. The actual death toll is likely much higher, with the capital's hospital overwhelmed and many dying at home, Greenwood said.
Only 12% of Solomon Islanders are fully vaccinated, though the outbreak has provided new impetus to the country's vaccination campaign and 29% now have at least one shot.
Global vaccine disparity continues, with only 6.95% of people in low-income countries fully vaccinated, compared to more than 73% in high-income nations, according to Our World in Data.
In a good sign, at the end of last month Africa surpassed Europe in the number of doses administered daily, but only about 12.5% of its population has received two shots.
The Africa Centers for Disease Control and Prevention is still pressing for more vaccines, though it has been a challenge. Some shipments arrive with little warning for countries' health systems and others near the expiration date—forcing doses to be destroyed.
Eastern Europe has been particularly hard hit by the omicron variant, and with the Russian invasion of Ukraine, a new risk has emerged as hundreds of thousands of people flee to places like Poland on crowded trains. Health officials there have been offering free vaccinations to all refugees, but have not been making them test upon arrival or quarantine.
"This is really tragic because great stress has a very negative effect on natural immunity and increases the risk of infections," said Anna Boron-Kaczmarska, a Polish infectious disease specialist. "They are in very high stress, being afraid for their lives, the lives of their children, they family members."
Mexico has reported 300,000 deaths, but with little testing, a government analysis of death certificates puts the real number closer to 500,000. Still, four weeks of falling infection rates have left health officials optimistic.
In India, where the world was shocked by images of open-air pyres of bodies burned as crematoria were overwhelmed, the scars are fading as the number of new cases and deaths has slowed.
India has recorded more than 500,000 deaths, but experts believe its true toll is in the millions, primarily from the delta variant. Migrants from India's vast hinterland are now returning to its megacities in search of jobs, and the streets are packed with traffic. Shopping malls have customers, albeit still masked, while schools and universities are welcoming students after a months-long gap.
In Britain, infections have fallen since an omicron-driven surge in December, but remain high. England has now lifted all restrictions, including mask mandates and the requirement that all who test positive isolate at home.
With about 250,000 reported deaths, the African continent's smaller death toll is thought to stem from underreporting, as well as a generally younger and less mobile population.
"Africa is a big question mark for me, because it has been relatively spared from the worst so far, but it could just be a time bomb," Pang said, noting its low vaccination rates.
In South Africa, Soweto resident Thoko Dube said she received news of the deaths of two family members on the same day in January 2021—a month before the country received its first vaccines.
It has been difficult, but "the family is coping," she said. "We have accepted it because it has been happening to other families."
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Heliobas Disciple
TB Fanatic
COVID Omicron Variant Detected for First Time in White-Tailed Deer
Detection of antibodies in one infected deer also suggests deer may become reinfected with SARS-CoV-2. Some white-tailed deer living in Staten Island, New York, are actively infected with the Omicron (B.1.1.529) variant of SARS-CoV-2, according to new research led by scientists at Penn State. The
scitechdaily.com
COVID Omicron Variant Detected for First Time in White-Tailed Deer
By Penn State University
March 6, 2022
Detection of antibodies in one infected deer also suggests deer may become reinfected with SARS-CoV-2.
Some white-tailed deer living in Staten Island, New York, are actively infected with the Omicron (B.1.1.529) variant of SARS-CoV-2, according to new research led by scientists at Penn State. The team also found neutralizing antibodies to SARS-CoV-2 in one of the Omicron-infected deer, suggesting that, like humans, deer can be reinfected with the virus.
“The deer population on Staten Island is so large that the animals are considered by local wildlife officials to pose significant challenges to human health and safety, particularly from vehicle collisions and the spread of tick-borne diseases,” said Kurt Vandegrift, associate research professor of biology, Penn State, and lead author of the paper, which published on the pre-print server bioRxiv in February. “Our finding that some of these animals harbor SARS-CoV-2 suggests the presence of another potential threat. This is particularly concerning because Staten Island represents a situation where a highly dense human population lives in close proximity to a large population of deer.”
Last fall, Suresh Kuchipudi, Huck Chair in Emerging Infectious Diseases and clinical professor of veterinary and biomedical sciences, Penn State, led a team — including Vandegrift and Vivek Kapur, Huck Distinguished Chair in Global Health and professor in the Department of Animal Science at Penn State — that found that up to 80% of white-tailed deer sampled across Iowa tested positive for SARS-CoV-2. The finding was the first direct evidence of SARS-CoV-2 virus in any free-living species.
According to Kuchipudi, the team’s latest research highlights that many urgent steps are needed to monitor the spread of the virus in deer and prevent potential spillback to humans.
“While there is no indication so far of any of the SARS-CoV-2 variants spilling back into humans from deer, such an outcome is possible,” said Kuchipudi. “The longer the virus circulates in these animals and the greater the number of individuals it infects, the more likely the virus is to evolve and potentially lead to the emergence of a completely novel variant that may be resistant to our current vaccines, which would be a serious problem if the virus were to spill back into humans. Our ongoing research in deer may at some point reveal whether spillover back to humans from this animal is possible.”
The team targeted Staten Island because of its close proximity to New York City, where Omicron infection rates at the time were high. The team partnered with scientists at the City of New York Department of Parks and Recreation Wildlife Unit, which is running a population control program for white-tailed deer.
The team analyzed blood samples from 131 individual deer collected between December 12, 2021, and January 31, 2022, and found that 19 were positive for SARS-CoV-2-specific antibodies. The team also detected SARS-CoV-2 nucleic acid in nasal swabs from seven of 68 of the sampled deer, indicating that these deer were actively infected with the virus.
“Our previous research in Iowa examined the lymph nodes of deer that had already been killed during hunting, but we were not able to confirm an active infection from these samples,” said Kapur, who helped co-lead the current study. “In our new study, we were able to obtain nasal swabs, which revealed live virus in the animals’ noses.”
Finally, whole-genome sequencing identified that the virus circulating among the white-tailed deer on Staten Island was Omicron. Phylogenetic analyses, which examine the evolutionary history among groups of organisms, revealed that the Omicron sequences in the deer were related to Omicron sequences recovered from infected humans in New York City and elsewhere, suggesting the virus spilled over from humans to deer.
“Importantly, one individual deer was both positive for viral RNA and had a high level of neutralizing antibodies, suggesting that neutralizing antibodies developed rapidly during an ongoing infection or that a breakthrough infection occurred,” said Kuchipudi. “If this animal had a reinfection, then this suggests that white-tailed deer can serve as a reservoir for the virus to continue to mutate, potentially producing new variants that are more dangerous.”
The team’s results also revealed a difference in antibody prevalence between age groups, where a significantly greater proportion of yearling deer, ages 12 to 24 months, possessed neutralizing antibodies than did fawns, which are less than 12 months old.
“Our finding of age-structure in antibody prevalence may help in finetuning future surveillance strategies,” said Vandegrift.
Reference: “Detection of SARS-CoV-2 Omicron variant (B.1.1.529) infection of white-tailed deer” by Kurt J. Vandegrift, Michele Yon, Meera Surendran-Nair, Abhinay Gontu, Saranya Amirthalingam, Ruth H. Nissly, Nicole Levine, Tod Stuber, Anthony J. DeNicola, Jason R. Boulanger, Nathan Kotschwar, Sarah Grimké Aucoin, Richard Simon, Katrina Toal, Randall J. Olsen, James J. Davis, Dashzeveg Bold, Natasha N. Gaudreault, Juergen A. Richt, James M. Musser, Peter J. Hudson, Vivek Kapur and Suresh V. Kuchipudi, 7 February 2022, bioRxiv.
DOI: 10.1101/2022.02.04.479189
Other Penn State authors on the paper include Michele Yon, research technologist in veterinary and biomedical sciences; Meera Surendran-Nair, assistant clinical professor in veterinary and biomedical sciences; Abhinay Gontu, graduate student in veterinary and biomedical sciences; Saranya Amirthalingam, graduate student in the Huck Institutes of the Life Science; Ruth Nissly, laboratory manager in veterinary and biomedical sciences; Nicole Levine, laboratory manager in veterinary and biomedical sciences; and Peter Hudson, Willaman Professor of Biology. Other authors include Tod Stuber, National Animal Disease Center, USDA; Anthony DeNicola, founder/CEO, White Buffalo Inc.; Jason Boulanger, president, White Buffalo Inc.; Nathan Kotschwar, veterinarian, White Buffalo Inc.; Sarah Grimké Aucoin, director of Urban Park Rangers, City of New York Department of Parks and Recreation; Richard Simon, wildlife unit director, City of New York Department of Parks and Recreation; Katrina Toal, wildlife unit deputy director, City of New York Department of Parks and Recreation; Randall Olsen, professor of clinical pathology and genomic medicine, Houston Methodist and Weill Cornell Medical College; James Davis, computational scientist, Argonne National Laboratory; Dashzeveg Bold, graduate student, Kansas State University; Natasha Gaudreault, research assistant professor, Kansas State University; Juergen Richt, Regents Distinguished Professor, Kansas State University; James Musser, professor of pathology and genomic medicine, Houston Methodist.
The U.S. Department of Agriculture National Institute of Food and Agriculture, National Science Foundation, National Institutes of Health and Huck Institutes of the Life Sciences at Penn State supported this research.
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Heliobas Disciple
TB Fanatic
Neem Tree Bark Extract May Protect Against COVID – Including Future Variants
New research reveals Neem-based drugs may help fight future coronavirus variants. Extract from the bark of the Neem tree may help treat and reduce the spread of coronavirus, according to a new study led by scientists at the University of Colorado Anschutz Medical Campus and the Indian Institute o
scitechdaily.com
Neem Tree Bark Extract May Protect Against COVID – Including Future Variants
By University of Colorado Anschutz Medical Campus
March 5, 2022
New research reveals Neem-based drugs may help fight future coronavirus variants.
Extract from the bark of the Neem tree may help treat and reduce the spread of coronavirus, according to a new study led by scientists at the University of Colorado Anschutz Medical Campus and the Indian Institute of Science Education and Research Kolkata.
The study, reported recently in the journal Virology, shows that components of Neem bark may target a wide range of viral proteins, suggesting its potential as an antiviral agent against emerging variants of coronaviruses (including SARS-CoV-2).
The Neem tree, indigenous to India, has been used for thousands of years for its anti-parasitic, anti-bacterial, and antiviral properties. The bark extract has helped treat malaria, stomach, and intestinal ulcers, skin diseases, and many other diseases.
Neem-based medications for treating emerging variants
“The goal of this research is to develop a Neem-based medication that can reduce the risk of serious illness when someone is infected with coronaviruses,” said study co-author Maria Nagel, MD, research professor in the department of neurology and ophthalmology at the University of Colorado School of Medicine on the CU Anschutz Medical Campus.
“We hope that scientists won’t have to continuously develop new therapies every time a new SARS-CoV-2 variant emerges,” she said. “Just like how we take penicillin for strep throat, we envision taking the Neem-based drug for COVID, allowing us to resume our normal lives without fear of hospitalization and death.”
The scientists investigated the impact of the bark extract against coronaviruses in their laboratories. In India, researchers tested it in animal models and showed that it had antiviral properties against coronavirus. Using computer modeling, the researchers predicted that Neem bark extract will bind to the SARS-CoV-2 spike protein at various locations, preventing virus entry to host cells.
At CU Anschutz, Nagel’s lab tested the Neem bark extract in SARS-CoV-2 human lung cells. It proved as effective as a preventive drug for infection and also decreased virus replication and spread after infection.
Combatting the ongoing pandemic
“The next step in our research is to identify the specific components in Neem bark extract that are antiviral. Because these components bind to various regions of SARS-CoV-2, we believe that it will be effective on emerging variants with spike mutations,” said Nagel. “We will then determine the formulation of dosage for an antiviral drug to treat coronavirus infections.”
The scientists said this research could guide new antiviral therapeutic efforts to combat the ongoing pandemic, while holding out the promise for treating new coronavirus strains.
Reference: “Azadirachta indica A. Juss bark extract and its Nimbin isomers restrict β-coronaviral infection and replication” Lucky Sarkar, Lauren Oko, Soham Gupta, Andrew N. Bubak, Bishnu Das, Parna Gupta, Abass Alao Safiriyu, Chirag Singhal, Ujjwal Neogi, David Bloom, Arup Banerjee, Ravi Mahalingam, Randall J. Cohrs, Michael Koval, Kenneth S. Shindler, Debnath Pal, Maria Nagel and Jayasri Das Sarma, 15 February 2022, Virology.
DOI: 10.1016/j.virol.2022.01.002
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marsh
On TB every waking moment
The Curtain Close on COVID
The Curtain Close on COVID
Governor DeSantis hosts a roundtable with physicians nationwide on ending COVID theater once and for all.
Please watch the Florida Surgeon General’s announcement about recommending against COVID-19 vaccines for children.
The Curtain Close on COVID Theater
Ron DeSantis Published March 7, 2022
On Rumble - https://rumble.com/vwposh-the-curtain-close-on-covid-theater.html 1:41:01 min
View: https://youtu.be/iulvEmAmtcQ
1:35:59 min
| Robert W Malone MD, MS
|
The Curtain Close on COVID
Governor DeSantis hosts a roundtable with physicians nationwide on ending COVID theater once and for all.
Please watch the Florida Surgeon General’s announcement about recommending against COVID-19 vaccines for children.
The Curtain Close on COVID Theater
Ron DeSantis Published March 7, 2022
On Rumble - https://rumble.com/vwposh-the-curtain-close-on-covid-theater.html 1:41:01 min
1:35:59 min
jward
passin' thru
Breaking911
@Breaking911
10m
JUST IN: Florida Dept. of Health to recommend against COVID-19 vaccine for healthy children, becoming the first state in the country to directly contradict guidance from the CDC - WPTV
@Breaking911
10m
JUST IN: Florida Dept. of Health to recommend against COVID-19 vaccine for healthy children, becoming the first state in the country to directly contradict guidance from the CDC - WPTV
marsh
On TB every waking moment
Joint Campaign Combs Through Thousands of Pfizer Documents
Joint Campaign Combs Through Thousands of Pfizer Documents
rumble.com
Joint Campaign Combs Through Thousands of Pfizer Documents (Naomi Wolf, PhD)
Bannons War Room Published March 7, 2022
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Emerald Robinson Reports on News Outlets Taking Money to Promote Covid Vaccine 8:28 min
Emerald Robinson Reports on News Outlets Taking Money to Promote Covid Vaccine
Bannons War Room Published March 7, 2022
marsh
On TB every waking moment
The State of Florida Officially Recommends Against the COVID-19 Vaccines for Healthy Children .18 min
The State of Florida Officially Recommends Against the COVID-19 Vaccines for Healthy Children
Red Voice Media Published March 7, 2022
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Candace Owens Interviews Dr. Robert Malone - Part 1 of 2 1:36:02 min
Candace Owens Interviews Dr. Robert Malone - Part 1 of 2
Sunfellow on COVID-19 Published March 7, 2022
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Candace Owens Interviews Dr. Robert Malone - Part 2 of 2 1:45:53 min
Candace Owens Interviews Dr. Robert Malone - Part 2 of 2
Sunfellow on COVID-19 Published March 7, 2022
The State of Florida Officially Recommends Against the COVID-19 Vaccines for Healthy Children
Red Voice Media Published March 7, 2022
^^^^
Candace Owens Interviews Dr. Robert Malone - Part 1 of 2 1:36:02 min
Candace Owens Interviews Dr. Robert Malone - Part 1 of 2
Sunfellow on COVID-19 Published March 7, 2022
^^^^
Candace Owens Interviews Dr. Robert Malone - Part 2 of 2 1:45:53 min
Candace Owens Interviews Dr. Robert Malone - Part 2 of 2
Sunfellow on COVID-19 Published March 7, 2022
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marsh
On TB every waking moment
Dr. McCullough: Less Than 20% Efficacy in Children—Severe Adverse Events 1:28 min
Dr. McCullough: Less Than 20% Efficacy in Children—Severe Adverse Events
Red Voice Media Published March 7, 2022
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Video Evidence Suggests Janet Woodcock and Rick Bright Suppressed HCQ to Enable EUA for the Vaccines 2:04 min
Video Evidence Suggests Janet Woodcock and Rick Bright Suppressed HCQ to Enable EUA for the Vaccines
Red Voice Media Published March 7, 2022
Dr. McCullough: Less Than 20% Efficacy in Children—Severe Adverse Events
Red Voice Media Published March 7, 2022
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Video Evidence Suggests Janet Woodcock and Rick Bright Suppressed HCQ to Enable EUA for the Vaccines 2:04 min
Video Evidence Suggests Janet Woodcock and Rick Bright Suppressed HCQ to Enable EUA for the Vaccines
Red Voice Media Published March 7, 2022
marsh
On TB every waking moment
There Is No Reason to Jab the Children—the FDA Failed to Do Its Job 2:32 min
There Is No Reason to Jab the Children—the FDA Failed to Do Its Job
Red Voice Media Published March 7, 2022
^^^
There Is No Reason to Jab the Children—the FDA Failed to Do Its Job
Red Voice Media Published March 7, 2022
^^^
Heliobas Disciple
TB Fanatic
/cloudfront-us-east-2.images.arcpublishing.com/reuters/4UWOFNROPJLIXJ2RIJ674VDRFI.jpg)
Scientists identify new gene differences in severe COVID patients
Scientists have pinpointed 16 new genetic variants in people who developed severe COVID-19 in a large study published on Monday that could help researchers develop treatments for very sick patients.
www.reuters.com
Scientists identify new gene differences in severe COVID patients
By Manas Mishra
March 7, 202211:06 AM EST Last Updated 10 hours ago
Scientists have pinpointed 16 new genetic variants in people who developed severe COVID-19 in a large study published on Monday that could help researchers develop treatments for very sick patients.
The results suggest that people with severe COVID have genes that predispose them to one of two problems: failure to limit the ability of the virus to make copies of itself, or excessive inflammation and blood clotting.
The scientists said their discoveries, published in the journal Nature, could help prioritise the likely treatments that could work against the disease.
Eventually, the information could even help predict which patients were likely to become severely ill.
"It is potentially possible in future that we will be able to make predictions about patients based on their genome at the point of presenting (for) critical care," said Kenneth Baillie, consultant in critical care medicine at the University of Edinburgh and one of the study authors, told reporters.
The genetic analysis of nearly 56,000 samples from people in Britain showed differences in 23 genes in COVID-19 patients who became critically ill, when compared with the DNA of other groups included in the study, including 16 differences that had not been previously identified.
The new findings could help guide scientists in their search for existing drugs that might be useful for treating COVID-19.
For example, the researchers found changes in key genes that regulate the level of factor VIII, a protein involved in forming blood clots.
"Blood clotting is one of the main reasons why patients with COVID develop a shortage of oxygen. So that's potentially targetable to prevent those clots from forming," Baillie said.
But "we can't know if these medicines will work until we try them in people".
One of the previously discovered genes, TYK2, is targeted by Eli Lilly's (LLY.N) arthritis drug baricitinib, now being studied as a treatment for COVID-19.
The drug was shown last week to cut the risk of death and hospitalisation in COVID-19 patients by 13% a trial. read more
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Heliobas Disciple
TB Fanatic
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Omicron infections contagious for at least 6 days; Takeda drug shows promise as COVID treatment
The following is a summary of some recent studies on COVID-19. They include research that warrants further study to corroborate the findings and that has yet to be certified by peer review.
www.reuters.com
Omicron infections contagious for at least 6 days; Takeda drug shows promise as COVID treatment
By Nancy Lapid
March 7, 20223:41 PM EST Last Updated 5 hours ago
March 7 (Reuters) - The following is a summary of some recent studies on COVID-19. They include research that warrants further study to corroborate the findings and that has yet to be certified by peer review.
Omicron infections are contagious for at least 6 days
Patients infected with the Omicron variant of SARS-CoV-2 remain contagious for just as long as patients infected with earlier variants, according to a small study.
Researchers took blood samples from 56 newly-diagnosed patients, including 37 with Delta infections and 19 with Omicron infections. All were mildly ill, such as with flu-like symptoms, but none were hospitalized. Regardless of which variant or whether or not they had been vaccinated or boosted, study participants "shed live virus for, on average, about 6 days after symptoms (began), and... about one in four people shed live virus for over 8 days," said Dr. Amy Barczak of the Massachusetts General Hospital in Boston, who coauthored a report posted on medRxiv ahead of peer review.
"Although it is unknown exactly how much live virus is needed to spread the disease to others, we take these data to suggest that people with mild COVID-19 infection may be contagious on average for 6 days, and sometimes longer," Barczak said. "Decisions about isolation and masking should take such information into account, regardless of variant or prior vaccination status."
Takeda angioedema drug shows promise for COVID-19
A drug used to treat a blood vessel condition called angioedema has shown promise as a treatment for COVID-19 in lab experiments, researchers said.
Icatibant, sold as Firazyr by Japan's Takeda Pharmaceutical Co (4502.T), blocks a protein called bradykinin receptor b2 in the so-called kinin system. The protein is regulated by the ACE2 protein on cell surfaces, which the coronavirus uses as a gateway for infection. When the researchers analyzed nasal cells obtained from newly diagnosed COVID-19 patients, they found elevated levels of bradykinin receptor b2, which led them to wonder whether blocking that protein with icatibant could protect the airway-lining cells against the coronavirus. "To our surprise, icatibant effectively reduced viral load by more than 90% and protected cultured human airway cells from cell death upon SARS-CoV-2-infection," said Adam Chaker of Technical University of Munich, whose team reported their findings on Saturday in the Journal of Molecular Medicine. Icatibant uses different biochemical pathways to protect the airways than steroids, the researchers found.
In their test tube experiments, repeated dosing of icatibant did not stop coronavirus infection completely, but reduced the severity of infection, they reported. Previous small observational studies have suggested that icatibant might provide some benefit to COVID-19 patients. Now, Chaker said, it is time for "double-blind, placebo-controlled clinical trials ... conducted in high-risk patients and see potential to use icatibant as add-on treatment at early stages of infection."
Heart defects boost risks for hospitalized COVID-19 patients
People born with heart defects who become sick enough from COVID-19 to be hospitalized are at higher risk for becoming critically ill or dying, researchers said.
The findings were drawn from a study that compared 421 patients with a heart defect who were hospitalized for COVID-19 with 235,638 similar hospitalized COVID-19 patients born with normal hearts. After researchers accounted for patients' other risk factors, those with congenital heart defects were 40% more likely to be admitted to an intensive care unit, 80% more likely to need mechanical ventilation, and two times more to die while hospitalized, compared to patients in the control group, according to the report published on Monday in the journal Circulation. Hospitalized patients with a congenital heart defect and another health condition faced even higher risks for poor outcomes, the researchers found.
"People with heart defects should be encouraged to receive the COVID-19 vaccines and boosters and to continue to practice additional preventive measures for COVID-19, such as mask-wearing and physical distancing," study leader Karrie Downing of the U.S. Centers for Disease Control and Prevention said in a statement.
Click for a Reuters graphic on vaccines in development.
.
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U.S. CDC urges Americans to avoid travel to Hong Kong, New Zealand
The Centers for Disease Control and Prevention (CDC) on Monday urged Americans to avoid travel to Hong Kong, New Zealand and Thailand over COVID-19 cases.
www.reuters.com
U.S. CDC urges Americans to avoid travel to Hong Kong, New Zealand
By David Shepardson
March 7, 20223:45 PM EST Last Updated 5 hours ago
WASHINGTON, March 7 (Reuters) - The Centers for Disease Control and Prevention (CDC) on Monday urged Americans to avoid travel to Hong Kong, New Zealand and Thailand over COVID-19 cases.
The CDC elevated its travel recommendation to "Level Four: Very High" for the three destinations. In total, the CDC urges Americans to avoid travel to about 135 countries and territories.
The CDC lists another 33 destinations as "Level 3: High" and recommends unvaccinated Americans avoid travel. It lowered six destinations on Monday to Level 3: Anguilla, Cape Verde, Fiji, Mexico, Philippines and United Arab Emirates. A total of just 29 destinations are listed as "Level 2: Moderate" or "Level 1: Low."
Hong Kong reported 25,150 new coronavirus infections and 280 deaths on Monday, as authorities struggle to contain a worsening COVID-19 outbreak which has torn through hundreds of nursing homes and hit many of the city's unvaccinated elderly.
While Hong Kong was successful in controlling the virus in 2021, COVID-19 infections there have recently soared to a total of around 500,000. Most of the Chinese-ruled city's more than 2,200 deaths have been in the past two weeks.
Hong Kong reported the most deaths globally per million people in the week to March 6, according to data publication Our World in Data. CDC raised Hong Kong to "Level 3" last week.
.
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Florida breaks with CDC, recommends no COVID vaccine for healthy children
Florida's top health official said on Monday the state would recommend against the COVID-19 vaccine for healthy children, breaking with guidance from the U.S. Centers for Disease Control and Prevention.
www.reuters.com
Florida breaks with CDC, recommends no COVID vaccine for healthy children
By Dan Whitcomb
March 7, 20225:33 PM EST Last Updated 3 hours ago
March 7 (Reuters) - Florida's top health official said on Monday the state would recommend against the COVID-19 vaccine for healthy children, breaking with guidance from the U.S. Centers for Disease Control and Prevention.
In announcing the move during press briefing convened by Florida Governor Ron DeSantis, the state's surgeon general Dr. Joseph Lapado cited studies that showed few COVID fatalities among healthy children and elevated risk among young boys receiving the vaccine of side effects such as myocarditis.
"The Florida Department of Health is going to be first state to officially recommend against the use of COVID 19 vaccines for healthy children," Lapado said during the more than 90-minute panel discussion.
Last week, a study based on New York state health records suggested that the Pfizer/BioNTech vaccine was less effective at preventing infection in children aged 5 to 11 than in older kids but still cut hospitalizations by about 50%. read more
A U.S. Centers for Disease Control and Prevention report released in January found that the vaccine was 91% effective in preventing rare but often serious conditions in children that causes organ inflammation weeks after COVID-19 infections called Multisystem Inflammatory Syndrome in Children in 12-18 year olds.
The CDC has strongly recommended that parents have children over the age of 5 inoculated, despite a sharp decline in infections and hospitalizations nationwide since a winter peak in January and evidence that it has been less effective against the Omicron variant.
"It's deeply disturbing that there are politicians peddling conspiracy theories out there and casting doubt on vaccinations when is our best tool against the virus and the best tool to prevent even teenagers from being hospitalized," White House spokeswoman Jen Psaki said in response to Lapado's comments.
DeSantis, a Republican often named as a potential 2024 presidential candidate, has often sparred with Biden, a Democrat, over COVID mandates and restrictions.
The CDC referred Reuters to their existing recommendation.
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Heliobas Disciple
TB Fanatic
Posting this for Profit of Doom:
boriquagato.substack.com
(fair use applies)
variant specific boosters fail to elicit variant specific response
did NIH researchers just prove the moderna vaccine leads to OAS?
el gato malo
13 hrs ago
THIS is a very interesting paper written by a bewilderingly large number of authors (66 in total), many from NIH and NIAID. it carries the somewhat technical and tepid title of:
it would, frankly, be quite easy to miss or dismiss as “oh, it’s just an equivalency study.” but this has some real juicy bits that were brought to my attention by long-term gatopal™ and all around good guy and standout bright spot at brown university medical school andrew bostom with whom i have had the good fortune to collaborate on a number of projects.
the researchers took a number of non human primates (NHP’s) and vaccinated them against covid using mRNA-1273 (the moderna vaccine).
they observed the now well known immunity fade out to 40 weeks, then boosted them in week 41 with either another dose of mRNA-1273 or with a variant specific dose called mRNA-Omicon that used the spike protein from the Omicron variant instead of the original.
the question was simple:
and so was the answer.
they worked out to be very much the same, so there was no benefit to a variant boost vs more of the old one. lots of studies cited to claim boosters are good (albeit far less so vs omicron and with rapid fade, counting only those doses +2 weeks for efficacy and ignoring/misallocating the immune suppression window) yadda yadda. so far, so boring.
but then it starts to get interesting because of what they may have accidentally proven (or deliberately investigated and then buried in technical reporting far away from the headlines). they found original antigenic sin (OAS, also known as hoskin’s effect).
well, NOW i’m interested.
it’s easy to miss the significance here if you’re not familiar with what you are looking at. what they are saying is that exposing you to the spike/s-1 proteins of omicron elicited no immune responses that diverged from the previous vaccine.
assuming (and i think this is likely a good assumption) that this vaccine accurately modeled omicron, this is a sign of antigenic fixation. you have locked your immune system into one set of responses and it is not learning new ones when faced with novel pathogen variants. (read OAS link above for details on how this works)
we can see the issue here:
this is a scatter of memory B cell specificities post immunization and boosting. think of B cells as a recipe storage medium. they are not the antibodies, they are the cells that remember which antibodies to make and how to make them.
it’s your immune memory.
these charts are a little tricky to read, so let’s walk through them:
the scatters break into 4 quadrants. upper left are B cells specific to the Y axis variant. lower right are B cells specific to the X axis variant. the upper right are effective on both.
look what happens here. you can see fade from week 6 to week 41 and then a resurgence in week 43 (post a week 41 boost)
now look at how different the responses to omi are vs traditional 1273.
not only is the response more muted, it’s FAR less broad. you’re getting far less B cell variety from the variant based booster, but more tellingly, it’s ALL a subset of the 1273 boost’s elicitations.
there is nothing new.
a new pathogen with more than 30 mutations on the S protein evoked NO new immune response. that is, to say the least, VERY suggestive. one might even go so far as to call it “outright worrying.”
it means your immune response has ceased to be trainable.
and this means you can get trapped, like this, in a suboptimal and increasingly ineffective immune response.
worse, it means that this response becomes a primary evolutionary selector for the virus. variants able to evade immunity without triggering a new adaptation will be selected for. rapidly. it’s not chance outcome that omicron was an OAS variant. it was the near inevitable outcomes of the selection pressure of antigenic fixation. (interestingly, omi looks to be a long throwback. it did not evolve from delta. it diverged from old strains before there even WAS a delta. this supports the idea that it was just a failed minor mutation until vaccines changed the playing field.)
this is a predicted and predictable outcome from leaky vaccines. (and one we’re seeing validated in UK data)
it’s actually WHY we don’t use leaky vaccines.
now, what would have been REALLY interesting is to do this same study but use actual omicron virus instead of boosters and to then compare the B cell map in vaccinated primates vs those who were vaccine naïve.
if the latter showed broader and more varied B cells, you’d know for sure you were dealing with an antigenically fixated population whose future immune development will be locked in place by overly narrow vaccines. this could, quite possibly, prevent long term sterilizing immunity from EVER developing in the vaccinated precisely BECAUSE they were vaccinated.
we’ve seen this in N antibodies already.
testing the effects of adaptive immune learning from exposure to live pathogen is a really obvious next step in an experimental series like this and one the researchers were well set up to undertake.
i wonder why they didn’t…?
.
variant specific boosters fail to elicit variant specific response
did NIH researchers just prove the moderna vaccine leads to OAS?
boriquagato.substack.com
variant specific boosters fail to elicit variant specific response
did NIH researchers just prove the moderna vaccine leads to OAS?
el gato malo
13 hrs ago
THIS is a very interesting paper written by a bewilderingly large number of authors (66 in total), many from NIH and NIAID. it carries the somewhat technical and tepid title of:
it would, frankly, be quite easy to miss or dismiss as “oh, it’s just an equivalency study.” but this has some real juicy bits that were brought to my attention by long-term gatopal™ and all around good guy and standout bright spot at brown university medical school andrew bostom with whom i have had the good fortune to collaborate on a number of projects.
the researchers took a number of non human primates (NHP’s) and vaccinated them against covid using mRNA-1273 (the moderna vaccine).
they observed the now well known immunity fade out to 40 weeks, then boosted them in week 41 with either another dose of mRNA-1273 or with a variant specific dose called mRNA-Omicon that used the spike protein from the Omicron variant instead of the original.
the question was simple:
and so was the answer.
they worked out to be very much the same, so there was no benefit to a variant boost vs more of the old one. lots of studies cited to claim boosters are good (albeit far less so vs omicron and with rapid fade, counting only those doses +2 weeks for efficacy and ignoring/misallocating the immune suppression window) yadda yadda. so far, so boring.
but then it starts to get interesting because of what they may have accidentally proven (or deliberately investigated and then buried in technical reporting far away from the headlines). they found original antigenic sin (OAS, also known as hoskin’s effect).
well, NOW i’m interested.
it’s easy to miss the significance here if you’re not familiar with what you are looking at. what they are saying is that exposing you to the spike/s-1 proteins of omicron elicited no immune responses that diverged from the previous vaccine.
assuming (and i think this is likely a good assumption) that this vaccine accurately modeled omicron, this is a sign of antigenic fixation. you have locked your immune system into one set of responses and it is not learning new ones when faced with novel pathogen variants. (read OAS link above for details on how this works)
we can see the issue here:
this is a scatter of memory B cell specificities post immunization and boosting. think of B cells as a recipe storage medium. they are not the antibodies, they are the cells that remember which antibodies to make and how to make them.
it’s your immune memory.
these charts are a little tricky to read, so let’s walk through them:
the scatters break into 4 quadrants. upper left are B cells specific to the Y axis variant. lower right are B cells specific to the X axis variant. the upper right are effective on both.
look what happens here. you can see fade from week 6 to week 41 and then a resurgence in week 43 (post a week 41 boost)
now look at how different the responses to omi are vs traditional 1273.
not only is the response more muted, it’s FAR less broad. you’re getting far less B cell variety from the variant based booster, but more tellingly, it’s ALL a subset of the 1273 boost’s elicitations.
there is nothing new.
a new pathogen with more than 30 mutations on the S protein evoked NO new immune response. that is, to say the least, VERY suggestive. one might even go so far as to call it “outright worrying.”
it means your immune response has ceased to be trainable.
and this means you can get trapped, like this, in a suboptimal and increasingly ineffective immune response.
worse, it means that this response becomes a primary evolutionary selector for the virus. variants able to evade immunity without triggering a new adaptation will be selected for. rapidly. it’s not chance outcome that omicron was an OAS variant. it was the near inevitable outcomes of the selection pressure of antigenic fixation. (interestingly, omi looks to be a long throwback. it did not evolve from delta. it diverged from old strains before there even WAS a delta. this supports the idea that it was just a failed minor mutation until vaccines changed the playing field.)
this is a predicted and predictable outcome from leaky vaccines. (and one we’re seeing validated in UK data)
it’s actually WHY we don’t use leaky vaccines.
now, what would have been REALLY interesting is to do this same study but use actual omicron virus instead of boosters and to then compare the B cell map in vaccinated primates vs those who were vaccine naïve.
if the latter showed broader and more varied B cells, you’d know for sure you were dealing with an antigenically fixated population whose future immune development will be locked in place by overly narrow vaccines. this could, quite possibly, prevent long term sterilizing immunity from EVER developing in the vaccinated precisely BECAUSE they were vaccinated.
we’ve seen this in N antibodies already.
testing the effects of adaptive immune learning from exposure to live pathogen is a really obvious next step in an experimental series like this and one the researchers were well set up to undertake.
i wonder why they didn’t…?
.
Last edited:
Heliobas Disciple
TB Fanatic
ALSO FROM PROFIT OF DOOM:
igorchudov.substack.com
(fair use applies)
How could Chinese Cave Bats pick the NGVEGF motif from Swine Flu Pandemic?
And how "flu vaccine" destroys kids natural protection
Igor Chudov
11 hr ago
A new study came out that looks at reasons why some people seem to NOT catch Covid-19:
It is very interesting by itself and shows many amazing facts that can be classified as “bombshells”.
We already know that Sars-Cov-2 has some unnatural and unlikely sequences picked up from HIV, as well as from a Moderna cancer patent. Those specific sequences, mind you, are not in some unused genetic detritus of the Sars-Cov-2 RNA genome, they are occupying crucially important locations of the genetic code, near the furin cleavage site!
The article that I am discussing picked one more interesting finding: Sars-Cov-2 encodes a peptide NGVEGF, which is ONLY present in “Swine Flu” of 2008-2009.
How could bats, sitting in Chinese caves, pick up a peptide from Swine Flu of 2008, is a little bit of a mystery to me. Here’s a picture of this peptide:
NGVEGF, in this picture, is on the tip of the coronavirus spike protein!
Just as the HIV motifs and Moderna cancer patent motifs, this NGVEGF peptide sits at the highly important location called “receptor binding domain”. Without the RBD proteins, the Sars-Cov-2 would not be able to bind to human cells and the pandemic that we are experiencing, very possibly, would not even be a thing. Thus, likely, NGVEGF is not a random genetic “accident”.
Flu Immunity
The authors of the article make a very straightforward point, saying that many people’s preexisting immunity to NGVEGF being present in flu infections that they experienced, may be the reason why the initial waves of Sars-Cov-2 infected only 20-23% of people.
It further lends credibility to the claim that NGVEGF (mysteriously transplanted from swine flu to Sars-Cov-2) is indeed contributing to protective immune reaction from people who had a flu with the same motif, in the past.
Of course, as we know, Sars-Cov-2 mutated later and was able to infect many more people, and the mutations also changed the NGVEGF peptide to evade prior flu immunity. But NGVEGF did its job in getting the pandemic started to infect 23% of people, after which the virus mutated.
Things get worse from here.
Flu Vaccine Detrimental to Children?
The other bombshell hypothesis from this article, is that “flu vaccination” in children likely leads to their decreased ability to protect against SARS-Cov-2.
It is not my plan to advocate for or against flu vaccine in this article, as it would likely be distracting from the overall message; but clearly, flu does interact with Covid in a very interesting way.
I, personally, would never consider a “flu vaccine” for myself or my children.
To other substack writers reading this post: this scientific article by Almazan et al, is likely a gold mine of other findings. I will be digging into it further but highly recommend that you look at it also. I would love to see you raise issues that I have not considered!
.
How could Chinese Cave Bats pick the NGVEGF motif from Swine Flu Pandemic?
And how "flu vaccine" destroys kids natural protection
igorchudov.substack.com
How could Chinese Cave Bats pick the NGVEGF motif from Swine Flu Pandemic?
And how "flu vaccine" destroys kids natural protection
Igor Chudov
11 hr ago
A new study came out that looks at reasons why some people seem to NOT catch Covid-19:
It is very interesting by itself and shows many amazing facts that can be classified as “bombshells”.
- Sars-Cov-2 contains a code to make NGVEGF peptide, that, incidentally, exists in H1N1 virus from the infamous “Swine Flu Pandemic”
- About 75-80% of people were immunologically protected from the original Sars-Cov-2
- Flu vaccination of children destroys or prevents immunity that they could enjoy against Sars-Cov-2
We already know that Sars-Cov-2 has some unnatural and unlikely sequences picked up from HIV, as well as from a Moderna cancer patent. Those specific sequences, mind you, are not in some unused genetic detritus of the Sars-Cov-2 RNA genome, they are occupying crucially important locations of the genetic code, near the furin cleavage site!
The article that I am discussing picked one more interesting finding: Sars-Cov-2 encodes a peptide NGVEGF, which is ONLY present in “Swine Flu” of 2008-2009.
How could bats, sitting in Chinese caves, pick up a peptide from Swine Flu of 2008, is a little bit of a mystery to me. Here’s a picture of this peptide:
NGVEGF, in this picture, is on the tip of the coronavirus spike protein!
Just as the HIV motifs and Moderna cancer patent motifs, this NGVEGF peptide sits at the highly important location called “receptor binding domain”. Without the RBD proteins, the Sars-Cov-2 would not be able to bind to human cells and the pandemic that we are experiencing, very possibly, would not even be a thing. Thus, likely, NGVEGF is not a random genetic “accident”.
Flu Immunity
The authors of the article make a very straightforward point, saying that many people’s preexisting immunity to NGVEGF being present in flu infections that they experienced, may be the reason why the initial waves of Sars-Cov-2 infected only 20-23% of people.
It further lends credibility to the claim that NGVEGF (mysteriously transplanted from swine flu to Sars-Cov-2) is indeed contributing to protective immune reaction from people who had a flu with the same motif, in the past.
Of course, as we know, Sars-Cov-2 mutated later and was able to infect many more people, and the mutations also changed the NGVEGF peptide to evade prior flu immunity. But NGVEGF did its job in getting the pandemic started to infect 23% of people, after which the virus mutated.
Things get worse from here.
Flu Vaccine Detrimental to Children?
The other bombshell hypothesis from this article, is that “flu vaccination” in children likely leads to their decreased ability to protect against SARS-Cov-2.
It is not my plan to advocate for or against flu vaccine in this article, as it would likely be distracting from the overall message; but clearly, flu does interact with Covid in a very interesting way.
I, personally, would never consider a “flu vaccine” for myself or my children.
To other substack writers reading this post: this scientific article by Almazan et al, is likely a gold mine of other findings. I will be digging into it further but highly recommend that you look at it also. I would love to see you raise issues that I have not considered!
.
Heliobas Disciple
TB Fanatic
Last one from Profit of Doom (so far 
) This is from March 2021, a year ago.
www.science.org
(fair use applies)
A call to arms
Researchers are testing an arsenal of weapons against the pandemic coronavirus.
Robert F. Service
11 Mar 2021
In March 2020, as the scope of the COVID-19 pandemic was coming into view, Jen Nwankwo and colleagues turned a pair of artificial intelligence (AI) tools against SARS-CoV-2. One newly developed AI program, called SUEDE, digitally screens all known druglike compounds for likely activity against biomolecules thought to be involved in disease. The other, BAGEL, predicts how to build inhibitors to known targets. The two programs searched for compounds able to block human enzymes that play essential roles in enabling the virus to infect our cells.
While SUEDE sifted through 14 billion compounds in just hours and spit out a hit, BAGEL made equally fast work of designing a lead. Nwankwo, CEO of a Massachusetts biotech startup called 1910 Genetics, asked a chemical company partner to synthesize the compounds. A week or so later, her team received the orders, added each compound in turn to human cells, and learned that each blocked its target and prevented viral entry into cells. 1910 Genetics is now looking to partner with antiviral drug developers to pursue animal and human trials. "It shows that AI can massively accelerate drug design," Nwankwo says.
Designing and developing a medicine is almost always painfully slow, regularly taking at least a decade. Many steps—such as animal studies, tweaking molecules to avoid side effects, and clinical trials—can't be accelerated. But the race toward new treatments against COVID-19 is off to a blistering start as researchers accelerate other parts of the search, deploying supercomputers, robots, synchrotrons, and every other tool they have to find and lab test possible medicines at speed. According to a biotech industry drug tracker, some 239 antiviral molecules against COVID-19 are under development, targeting multiple parts of the viral life cycle.
Antivirals have proved critical in fighting other infections such as HIV and hepatitis C. Such drugs will be vital in the struggle against the pandemic coronavirus, too, despite the ongoing rollout of COVID-19 vaccines. "We know not everyone will be able to take the vaccine or respond to it," says Mark Denison, a virologist at Vanderbilt University. Vaccines may also lose effectiveness as immune protection wanes or viral variants emerge. "So, continuing development of antivirals is critical," Denison says.
To date, most of that search has centered on "repurposed" compounds, antivirals originally developed to combat other diseases. (Other repurposed drugs, such as the steroid dexamethasone, target the body's reaction to infection rather than the virus itself.) "Drug repurposing made sense as the first thing to try," Nwankwo says. Many repurposed antivirals have shown promise against SARS-CoV-2 in cell and animal studies and are now in clinical trials. One, remdesivir, has already proved to speed recovery by a few days in very ill people. But several other repurposed antivirals have failed to prove effective.
As a result, says Francis Collins, director of the National Institutes of Health (NIH), "We really, really need a bunch more [antivirals]." Buoyed by almost daily advances in understanding SARS-CoV-2, the rapidly growing list of new compounds that might block it, and ongoing clinical trials—some of them late stage—Denison and others hope to deliver effective drugs this year. Says Andrew Mesecar, a structural biologist from Purdue University: "I am confident we will have more treatments for coronavirus."
As viruses go, SARS-CoV-2 is a behemoth, with some 30,000 letters of RNA in its genetic code. Those letters encode 29 viral proteins that enable the virus to infect cells, reproduce, escape, and spread. "We're fortunate this virus has provided us with so many targets, so many opportunities for intervention," says Sandra Weller, a molecular biologist at UConn Health.
The 29 proteins come in three main categories: structural proteins that make up the outer coat; nonstructural proteins (NSPs), most of which help the virus replicate; and accessory proteins, several of which appear to subdue the host's immune response. Thus far, drug hunters have taken aim mainly at the structural and replication proteins, concentrating on molecules similar to those that have paid off in fighting other viruses.
SARS-CoV-2 has just four structural proteins. The envelope and membrane proteins make up the virus' spherical shell, and the nucleocapsid protein shields its genome. The fourth protein, spike, protrudes from the shell, creating the crown of thorns that gives the virus its name and enables it to bind to angiotensin-converting enzyme 2 (ACE2) receptors, its main entry point into cells.
Spike is the primary target of many vaccines and antivirals. However, small molecules, the typical focus for drug discovery programs, won't work because they aren't bulky enough to prevent spike from binding to the ACE2 receptor.
David Baker, a computational biologist at the University of Washington, Seattle, and colleagues turned instead to miniproteins, each with about 60 amino acids, customized to block protein-protein interactions. In late 2020, Baker's team described miniproteins tailormade to bind tightly to the virus' spike protein and block it from attaching to the ACE2 receptor. The tiny proteins kept the virus from infecting human cells in a test tube, and Baker says miniproteins could make ideal drugs because they are far more stable than conventional protein therapeutics, such as antibodies, which must be refrigerated. Baker is in discussions with drug companies to pursue his leads.
Other researchers have a different strategy for interfering with viral binding. They are designing ACE2 look-alikes to serve as decoys, drawing SARS-CoV-2 away from cells. Researchers at Neoleukin Therapeutics and their partners, for example, reported creating a miniprotein, CTC-445.2d, that mimics ACE2, binding tenaciously to spike. The compound protected human cells from infection in vitro. When given to hamsters in a nasal spray, the decoy also prevented them from getting severe disease after they received a normally lethal dose of the virus. Another "receptor trap" molecule, described in November 2020 in the Proceedings of the National Academy of Sciences, also diverted SARS-CoV-2, keeping it from infecting cells in the test tube.
After entering a cell, a virus transforms its host into a virus factory. That's where SARS-CoV-2's NSPs come in. The viral proteins are made by the host cell's own protein factories, the ribosomes, which translate the viral RNA into two long "polyprotein" chains. The chains spin off two smaller proteins, NSP3 and NSP5, protein-cutting protease enzymes that then chop up the rest of the polyproteins into independent, functioning proteins.
"These are absolutely critical functions that are highly conserved and should be very, very vulnerable" to antivirals, Denison says.
Drugs that block proteases have successfully fought HIV and hepatitis C and have been among the most popular candidate antivirals for SARS-CoV-2. Two repurposed protease inhibitors for treating HIV, lopinavir and ritonavir, showed promise in vitro against SARS-CoV-2, but in October 2020, the United Kingdom's large Recovery clinical trial reported they offered no benefit.
[CONTINUED BELOW]
.
) This is from March 2021, a year ago.Science | AAAS
www.science.org
A call to arms
Researchers are testing an arsenal of weapons against the pandemic coronavirus.
Robert F. Service
11 Mar 2021
In March 2020, as the scope of the COVID-19 pandemic was coming into view, Jen Nwankwo and colleagues turned a pair of artificial intelligence (AI) tools against SARS-CoV-2. One newly developed AI program, called SUEDE, digitally screens all known druglike compounds for likely activity against biomolecules thought to be involved in disease. The other, BAGEL, predicts how to build inhibitors to known targets. The two programs searched for compounds able to block human enzymes that play essential roles in enabling the virus to infect our cells.
While SUEDE sifted through 14 billion compounds in just hours and spit out a hit, BAGEL made equally fast work of designing a lead. Nwankwo, CEO of a Massachusetts biotech startup called 1910 Genetics, asked a chemical company partner to synthesize the compounds. A week or so later, her team received the orders, added each compound in turn to human cells, and learned that each blocked its target and prevented viral entry into cells. 1910 Genetics is now looking to partner with antiviral drug developers to pursue animal and human trials. "It shows that AI can massively accelerate drug design," Nwankwo says.
Designing and developing a medicine is almost always painfully slow, regularly taking at least a decade. Many steps—such as animal studies, tweaking molecules to avoid side effects, and clinical trials—can't be accelerated. But the race toward new treatments against COVID-19 is off to a blistering start as researchers accelerate other parts of the search, deploying supercomputers, robots, synchrotrons, and every other tool they have to find and lab test possible medicines at speed. According to a biotech industry drug tracker, some 239 antiviral molecules against COVID-19 are under development, targeting multiple parts of the viral life cycle.
Antivirals have proved critical in fighting other infections such as HIV and hepatitis C. Such drugs will be vital in the struggle against the pandemic coronavirus, too, despite the ongoing rollout of COVID-19 vaccines. "We know not everyone will be able to take the vaccine or respond to it," says Mark Denison, a virologist at Vanderbilt University. Vaccines may also lose effectiveness as immune protection wanes or viral variants emerge. "So, continuing development of antivirals is critical," Denison says.
To date, most of that search has centered on "repurposed" compounds, antivirals originally developed to combat other diseases. (Other repurposed drugs, such as the steroid dexamethasone, target the body's reaction to infection rather than the virus itself.) "Drug repurposing made sense as the first thing to try," Nwankwo says. Many repurposed antivirals have shown promise against SARS-CoV-2 in cell and animal studies and are now in clinical trials. One, remdesivir, has already proved to speed recovery by a few days in very ill people. But several other repurposed antivirals have failed to prove effective.
As a result, says Francis Collins, director of the National Institutes of Health (NIH), "We really, really need a bunch more [antivirals]." Buoyed by almost daily advances in understanding SARS-CoV-2, the rapidly growing list of new compounds that might block it, and ongoing clinical trials—some of them late stage—Denison and others hope to deliver effective drugs this year. Says Andrew Mesecar, a structural biologist from Purdue University: "I am confident we will have more treatments for coronavirus."
As viruses go, SARS-CoV-2 is a behemoth, with some 30,000 letters of RNA in its genetic code. Those letters encode 29 viral proteins that enable the virus to infect cells, reproduce, escape, and spread. "We're fortunate this virus has provided us with so many targets, so many opportunities for intervention," says Sandra Weller, a molecular biologist at UConn Health.
The 29 proteins come in three main categories: structural proteins that make up the outer coat; nonstructural proteins (NSPs), most of which help the virus replicate; and accessory proteins, several of which appear to subdue the host's immune response. Thus far, drug hunters have taken aim mainly at the structural and replication proteins, concentrating on molecules similar to those that have paid off in fighting other viruses.
SARS-CoV-2 has just four structural proteins. The envelope and membrane proteins make up the virus' spherical shell, and the nucleocapsid protein shields its genome. The fourth protein, spike, protrudes from the shell, creating the crown of thorns that gives the virus its name and enables it to bind to angiotensin-converting enzyme 2 (ACE2) receptors, its main entry point into cells.
Spike is the primary target of many vaccines and antivirals. However, small molecules, the typical focus for drug discovery programs, won't work because they aren't bulky enough to prevent spike from binding to the ACE2 receptor.
David Baker, a computational biologist at the University of Washington, Seattle, and colleagues turned instead to miniproteins, each with about 60 amino acids, customized to block protein-protein interactions. In late 2020, Baker's team described miniproteins tailormade to bind tightly to the virus' spike protein and block it from attaching to the ACE2 receptor. The tiny proteins kept the virus from infecting human cells in a test tube, and Baker says miniproteins could make ideal drugs because they are far more stable than conventional protein therapeutics, such as antibodies, which must be refrigerated. Baker is in discussions with drug companies to pursue his leads.
Other researchers have a different strategy for interfering with viral binding. They are designing ACE2 look-alikes to serve as decoys, drawing SARS-CoV-2 away from cells. Researchers at Neoleukin Therapeutics and their partners, for example, reported creating a miniprotein, CTC-445.2d, that mimics ACE2, binding tenaciously to spike. The compound protected human cells from infection in vitro. When given to hamsters in a nasal spray, the decoy also prevented them from getting severe disease after they received a normally lethal dose of the virus. Another "receptor trap" molecule, described in November 2020 in the Proceedings of the National Academy of Sciences, also diverted SARS-CoV-2, keeping it from infecting cells in the test tube.
After entering a cell, a virus transforms its host into a virus factory. That's where SARS-CoV-2's NSPs come in. The viral proteins are made by the host cell's own protein factories, the ribosomes, which translate the viral RNA into two long "polyprotein" chains. The chains spin off two smaller proteins, NSP3 and NSP5, protein-cutting protease enzymes that then chop up the rest of the polyproteins into independent, functioning proteins.
"These are absolutely critical functions that are highly conserved and should be very, very vulnerable" to antivirals, Denison says.
Drugs that block proteases have successfully fought HIV and hepatitis C and have been among the most popular candidate antivirals for SARS-CoV-2. Two repurposed protease inhibitors for treating HIV, lopinavir and ritonavir, showed promise in vitro against SARS-CoV-2, but in October 2020, the United Kingdom's large Recovery clinical trial reported they offered no benefit.
[CONTINUED BELOW]
.
Heliobas Disciple
TB Fanatic
[CONTINUED]
Researchers at the drug giant Pfizer are pursuing an inhibitor that may work better because it is designed to target NSP5, a protease that is specific to SARS-CoV-2 and its coronavirus relatives. Pfizer scientists developed the drug in 2003 to block the molecule, also known as main protease (Mpro), in severe acute respiratory syndrome (SARS), the deadly coronavirus that emerged the previous year. That work was set aside when the SARS epidemic died out. Now, Pfizer has pulled the compound off the shelf and found that it stops SARS-CoV-2 from reproducing inside human cells. Pfizer researchers tweaked the structure to make a more soluble version, known as PF-07304814. They showed that it sharply reduced viral load in mice; in other animals, high concentrations of the drug could reach tissues.
"It's a promising lead," says Celia Schiffer, a molecular biologist with the University of Massachusetts Medical School. In September 2020, Pfizer launched a small clinical trial to test the safety of PF-07304814, delivered intravenously. But Annaliesa Anderson, who leads Pfizer's antiviral program, says recruiting volunteers has been difficult. "Patients are either very sick, and it might be too late [to inhibit viral replication], or they might not feel that bad," making an intravenous therapy less appealing. Given the slow recruitment, she expects results toward the end of this year.
Other researchers are also working on Mpro inhibitors. In Nature Communications in September 2020, researchers in China reported on two repurposed drugs, boceprevir and GC376. Boceprevir is a hepatitis C drug, whereas GC376 was designed to target a feline coronavirus. Both compounds slowed SARS-CoV-2 replication in cells. On 5 February, U.S. researchers reported in a bioRxiv preprint that most mice given GC376 after receiving a lethal dose of the pandemic virus survived. And in August 2020 in Science Translational Medicine, U.S. researchers described a GC376 analog that dramatically boosted survival rates in mice infected with Middle East respiratory syndrome and showed potent antiviral effects against SARS-CoV-2 in cells.
Other molecules designed specifically to inhibit SARS-CoV-2's Mpro remain at an earlier testing stage. In November 2020, for example, Charlotte Lanteri, a research microbiologist at the Walter Reed Army Institute of Research, reported discovering 807 Mpro inhibitors through an AI screen of 41 million compounds. Her team has identified seven as particularly promising, but turning one or more of those into drugs remains at least a couple of years away, says Lanteri, who reported the findings at an antiviral drug summit at NIH. She and colleagues are also looking for antiviral drugs effective against all coronaviruses. "We want to be prepared as much as possible for the next emerging threat," she says.
After SARS-CoV-2's proteases have freed coronavirus proteins from the original chains, 15 of them come together to form the replication transcription complex (RTC), which copies the virus' RNA genome to make new viruses (see graphic, above). Central to that machinery are NSP9, which locks onto the virus' RNA strand, and the RNA-dependent RNA polymerase (RdRp) that copies the RNA.
The RTC's critical role has made it, and RdRp in particular, the most popular treatment bull's-eye of all. It's where remdesivir does its work. The drug is a nucleoside analog, a sort of imitation RNA building block that resembles adenosine (A), one of the four letters that make up RNA. The imposter tricks the RdRp into inserting remdesivir molecules instead of A's into growing RNA strands, jamming RdRp and stopping viral replication.
Researchers hope other repurposed nucleoside and nucleotide analogs will be better at fooling the coronavirus' RdRp. (Nucleotides are nucleosides with one or more phosphate groups added.) The candidates include favipiravir and triazavirin, both originally designed to combat flu viruses; ribavirin, a treatment for respiratory syncytial virus and hepatitis C; and galidesivir, which can block replication of Ebola, Zika, and yellow fever viruses.
Researchers are guardedly optimistic about molnupiravir, a nucleoside analog that can be taken as a pill and was originally developed to combat influenza. Last year, concerns swirled around the drug after a whistleblower criticized what he saw as an improper effort to steer federal funding to it. But positive results have kept progress on track.
Early work showed molnupiravir inserts itself into RNA in place of the nucleoside cytidine, prompting errors in the copying process and causing a lethal buildup of mutations in the virus. That mechanism has raised worries that the drug might cause similar mutations in host cells. But Richard Plemper, a cell biologist at Georgia State University, says such problems have not been seen in animal studies.
In April 2020 in Science Translational Medicine, Denison and colleagues reported that in mice, molnupiravir sharply reduced replication of multiple coronaviruses, including SARS-CoV-2; the drug also cut SARS-CoV-2 replication in human airway epithelial cells. A Nature paper added to the encouraging data in February, showing the compound decreased viral replication 100,000-fold in mice engineered to have human lung tissue.
In December 2020, Plemper and colleagues reported in Nature Microbiology that molnupiravir might do more than just prevent symptoms. The researchers gave the drug to ferrets, which readily spread the coronavirus, and transmission fell to zero within 24 hours. "This is the first demonstration of an orally available drug to rapidly block SARS-CoV-2 transmission," Plemper says. That's crucial to slowing the spread of disease. Because it is a pill, molnupiravir can be given early in the disease cycle, just when SARS-CoV-2 replication typically peaks, in contrast to injectable drugs such as remdesivir. "We want to start treatment early and prevent people from ever showing up in a hospital," Plemper says.
The same month, a medRxiv preprint reported that a small safety trial showed the drug was well tolerated, with no serious side effects in healthy volunteers. Molnupiravir is now in phase 2/3 clinical trials run by Merck and Ridgeback Biotherapeutics; in March, scientists reported at a meeting that molnupiravir reduced patients' viral levels.
AT-527, another oral nucleoside analog developed to treat hepatitis C by Atea Pharmaceuticals and Roche, is also in a phase 2 clinical trial against COVID-19.
Scientists are trying to shut down other RTC proteins, too. In recent results, two compounds—zotatifin and plitidepsin—appear to block viral replication by interfering with NSP9, the RNA-grabbing enzyme. Plitidepsin is in a phase 2/3 trial by the Spanish drug company PharmaMar. At least three other NSPs are considered good targets, says Tomáš Cihlář, a virologist with Gilead Sciences, maker of remdesivir.
Eventually, drugs could target the coronavirus' RNA, not just its proteins. In Nature Biotechnology in February, Emmeline Blanchard, a biomedical engineer at the Georgia Institute of Technology, and colleagues reported creating a polymer-encased formulation of a gene-editing enzyme called Cas13a that seeks out and chops up snippets of SARS-CoV-2 RNA. The team's Cas13a enzyme targets highly conserved regions of two viral genes encoding the RdRp enzyme and the nucleocapsid protein. When hamsters infected with SARS-CoV-2 inhaled a vaporized formulation of the drug, it reduced viral replication and disease symptoms.
And in September 2020 in ACS Central Science, Matthew Disney, a chemist at the Scripps Research Institute, and colleagues reported discovering a compound called C5 that blocks a short, hairpin-shaped segment of RNA involved in SARS-CoV-2 replication. "We have other segments of the viral genome we think we can target as well," he says.
Because SARS-CoV-2 relies on a host cell's proteins to reproduce, disrupting those proteins could be another avenue to treatments—with the advantage that not targeting the virus directly could lower its odds of becoming resistant to the drugs. Their targets include host cell proteases TMPRSS2 and furin, which the candidate drugs from Nwankwo's team block. Last month, NIH announced it was launching a phase 2/3 trial for camostat mesilate, another TMPRSS2 inhibitor.
Another target is a protein called dihydroorotate dehydrogenase (DHODH). It's the linchpin in a pathway that cells use to make two of RNA's four bases when they need extra RNA—for example, when proliferating. Viruses hijack that pathway to replicate. In cell studies, blocking DHODH has halted cancer and viral diseases, such as influenza and cytomegalovirus. And DHODH blockers have thus far proved safe when tested in hundreds of patients.
Two biotech companies, PTC Therapeutics and Immunic Therapeutics, are trying the same strategy against SARS-CoV-2. Rapidly reproducing viruses "have a great need for RNA," says Marla Weetall, vice president of pharmacology with PTC Therapeutics. The company's compound, PTC299, was originally designed as an oral drug to halt cell proliferation in acute myeloid leukemia. In an August 2020 preprint on bioRxiv, Weetall and colleagues reported that PTC299 sharply inhibited SARS-CoV-2 replication in cells. The compound also blocked the production of immune molecules that cells build using RNA bases, hinting that PTC299 might help tame the immune overreaction seen in severe COVID-19.
Daniel Vitt, CEO of Immunic Therapeutics, says his company has also seen promising results in human trials of its oral compound, IMU-838, developed to treat inflammatory and autoimmune diseases. In February, the company reported preliminary results suggesting hospitalized patients on the drug had less need for ventilators. Trials continue for both companies.
Ultimately, no one compound is likely to deliver a knockout punch to the pandemic coronavirus, in part because drug-resistant viruses are likely to emerge. Collins and others argue that the best strategy takes a page from the treatment for HIV and hepatitis C: mixing and matching antivirals aimed at several proteins, making it harder for the virus to evolve multiple workarounds at once. "We really need an arsenal," says Lillian Chiang, CEO of Evrys Bio, which is working on antivirals against host-cell proteins.
"This is going to take time," says Michael Sofia, a chief scientific officer with Arbutus Biopharma, a Canadian antiviral company. And money. According to recent estimates, bringing a new drug to market costs between $985 million and $2.8 billion. Anderson says Pfizer, for one, is committing company resources to defeating the pandemic without expectation of profit. Other companies say the same. But during previous lulls in infectious disease outbreaks, many drug companies abandoned work on antivirals. "As soon as this stops being a hot area, people will move on," Nwankwo says.
In another disincentive, antiviral treatments for SARS-CoV-2 might be given for only a week or two, giving drugmakers a narrow window to reap returns. As a result, Denison and others argue that more government support is needed to keep stocking the antiviral arsenal. Any lull in the battle against SARS-CoV-2 and its kin is likely to be temporary, they say.
"We are going to have another coronavirus," Mesecar says. "We just don't know what it will look like."
*Clarification, 11 March, 2:30 p.m.: This story has been updated to clarify a whistleblower's allegation.
.
Researchers at the drug giant Pfizer are pursuing an inhibitor that may work better because it is designed to target NSP5, a protease that is specific to SARS-CoV-2 and its coronavirus relatives. Pfizer scientists developed the drug in 2003 to block the molecule, also known as main protease (Mpro), in severe acute respiratory syndrome (SARS), the deadly coronavirus that emerged the previous year. That work was set aside when the SARS epidemic died out. Now, Pfizer has pulled the compound off the shelf and found that it stops SARS-CoV-2 from reproducing inside human cells. Pfizer researchers tweaked the structure to make a more soluble version, known as PF-07304814. They showed that it sharply reduced viral load in mice; in other animals, high concentrations of the drug could reach tissues.
"It's a promising lead," says Celia Schiffer, a molecular biologist with the University of Massachusetts Medical School. In September 2020, Pfizer launched a small clinical trial to test the safety of PF-07304814, delivered intravenously. But Annaliesa Anderson, who leads Pfizer's antiviral program, says recruiting volunteers has been difficult. "Patients are either very sick, and it might be too late [to inhibit viral replication], or they might not feel that bad," making an intravenous therapy less appealing. Given the slow recruitment, she expects results toward the end of this year.
Other researchers are also working on Mpro inhibitors. In Nature Communications in September 2020, researchers in China reported on two repurposed drugs, boceprevir and GC376. Boceprevir is a hepatitis C drug, whereas GC376 was designed to target a feline coronavirus. Both compounds slowed SARS-CoV-2 replication in cells. On 5 February, U.S. researchers reported in a bioRxiv preprint that most mice given GC376 after receiving a lethal dose of the pandemic virus survived. And in August 2020 in Science Translational Medicine, U.S. researchers described a GC376 analog that dramatically boosted survival rates in mice infected with Middle East respiratory syndrome and showed potent antiviral effects against SARS-CoV-2 in cells.
Other molecules designed specifically to inhibit SARS-CoV-2's Mpro remain at an earlier testing stage. In November 2020, for example, Charlotte Lanteri, a research microbiologist at the Walter Reed Army Institute of Research, reported discovering 807 Mpro inhibitors through an AI screen of 41 million compounds. Her team has identified seven as particularly promising, but turning one or more of those into drugs remains at least a couple of years away, says Lanteri, who reported the findings at an antiviral drug summit at NIH. She and colleagues are also looking for antiviral drugs effective against all coronaviruses. "We want to be prepared as much as possible for the next emerging threat," she says.
After SARS-CoV-2's proteases have freed coronavirus proteins from the original chains, 15 of them come together to form the replication transcription complex (RTC), which copies the virus' RNA genome to make new viruses (see graphic, above). Central to that machinery are NSP9, which locks onto the virus' RNA strand, and the RNA-dependent RNA polymerase (RdRp) that copies the RNA.
The RTC's critical role has made it, and RdRp in particular, the most popular treatment bull's-eye of all. It's where remdesivir does its work. The drug is a nucleoside analog, a sort of imitation RNA building block that resembles adenosine (A), one of the four letters that make up RNA. The imposter tricks the RdRp into inserting remdesivir molecules instead of A's into growing RNA strands, jamming RdRp and stopping viral replication.
Researchers hope other repurposed nucleoside and nucleotide analogs will be better at fooling the coronavirus' RdRp. (Nucleotides are nucleosides with one or more phosphate groups added.) The candidates include favipiravir and triazavirin, both originally designed to combat flu viruses; ribavirin, a treatment for respiratory syncytial virus and hepatitis C; and galidesivir, which can block replication of Ebola, Zika, and yellow fever viruses.
Researchers are guardedly optimistic about molnupiravir, a nucleoside analog that can be taken as a pill and was originally developed to combat influenza. Last year, concerns swirled around the drug after a whistleblower criticized what he saw as an improper effort to steer federal funding to it. But positive results have kept progress on track.
Early work showed molnupiravir inserts itself into RNA in place of the nucleoside cytidine, prompting errors in the copying process and causing a lethal buildup of mutations in the virus. That mechanism has raised worries that the drug might cause similar mutations in host cells. But Richard Plemper, a cell biologist at Georgia State University, says such problems have not been seen in animal studies.
In April 2020 in Science Translational Medicine, Denison and colleagues reported that in mice, molnupiravir sharply reduced replication of multiple coronaviruses, including SARS-CoV-2; the drug also cut SARS-CoV-2 replication in human airway epithelial cells. A Nature paper added to the encouraging data in February, showing the compound decreased viral replication 100,000-fold in mice engineered to have human lung tissue.
In December 2020, Plemper and colleagues reported in Nature Microbiology that molnupiravir might do more than just prevent symptoms. The researchers gave the drug to ferrets, which readily spread the coronavirus, and transmission fell to zero within 24 hours. "This is the first demonstration of an orally available drug to rapidly block SARS-CoV-2 transmission," Plemper says. That's crucial to slowing the spread of disease. Because it is a pill, molnupiravir can be given early in the disease cycle, just when SARS-CoV-2 replication typically peaks, in contrast to injectable drugs such as remdesivir. "We want to start treatment early and prevent people from ever showing up in a hospital," Plemper says.
The same month, a medRxiv preprint reported that a small safety trial showed the drug was well tolerated, with no serious side effects in healthy volunteers. Molnupiravir is now in phase 2/3 clinical trials run by Merck and Ridgeback Biotherapeutics; in March, scientists reported at a meeting that molnupiravir reduced patients' viral levels.
AT-527, another oral nucleoside analog developed to treat hepatitis C by Atea Pharmaceuticals and Roche, is also in a phase 2 clinical trial against COVID-19.
Scientists are trying to shut down other RTC proteins, too. In recent results, two compounds—zotatifin and plitidepsin—appear to block viral replication by interfering with NSP9, the RNA-grabbing enzyme. Plitidepsin is in a phase 2/3 trial by the Spanish drug company PharmaMar. At least three other NSPs are considered good targets, says Tomáš Cihlář, a virologist with Gilead Sciences, maker of remdesivir.
Eventually, drugs could target the coronavirus' RNA, not just its proteins. In Nature Biotechnology in February, Emmeline Blanchard, a biomedical engineer at the Georgia Institute of Technology, and colleagues reported creating a polymer-encased formulation of a gene-editing enzyme called Cas13a that seeks out and chops up snippets of SARS-CoV-2 RNA. The team's Cas13a enzyme targets highly conserved regions of two viral genes encoding the RdRp enzyme and the nucleocapsid protein. When hamsters infected with SARS-CoV-2 inhaled a vaporized formulation of the drug, it reduced viral replication and disease symptoms.
And in September 2020 in ACS Central Science, Matthew Disney, a chemist at the Scripps Research Institute, and colleagues reported discovering a compound called C5 that blocks a short, hairpin-shaped segment of RNA involved in SARS-CoV-2 replication. "We have other segments of the viral genome we think we can target as well," he says.
Because SARS-CoV-2 relies on a host cell's proteins to reproduce, disrupting those proteins could be another avenue to treatments—with the advantage that not targeting the virus directly could lower its odds of becoming resistant to the drugs. Their targets include host cell proteases TMPRSS2 and furin, which the candidate drugs from Nwankwo's team block. Last month, NIH announced it was launching a phase 2/3 trial for camostat mesilate, another TMPRSS2 inhibitor.
Another target is a protein called dihydroorotate dehydrogenase (DHODH). It's the linchpin in a pathway that cells use to make two of RNA's four bases when they need extra RNA—for example, when proliferating. Viruses hijack that pathway to replicate. In cell studies, blocking DHODH has halted cancer and viral diseases, such as influenza and cytomegalovirus. And DHODH blockers have thus far proved safe when tested in hundreds of patients.
Two biotech companies, PTC Therapeutics and Immunic Therapeutics, are trying the same strategy against SARS-CoV-2. Rapidly reproducing viruses "have a great need for RNA," says Marla Weetall, vice president of pharmacology with PTC Therapeutics. The company's compound, PTC299, was originally designed as an oral drug to halt cell proliferation in acute myeloid leukemia. In an August 2020 preprint on bioRxiv, Weetall and colleagues reported that PTC299 sharply inhibited SARS-CoV-2 replication in cells. The compound also blocked the production of immune molecules that cells build using RNA bases, hinting that PTC299 might help tame the immune overreaction seen in severe COVID-19.
Daniel Vitt, CEO of Immunic Therapeutics, says his company has also seen promising results in human trials of its oral compound, IMU-838, developed to treat inflammatory and autoimmune diseases. In February, the company reported preliminary results suggesting hospitalized patients on the drug had less need for ventilators. Trials continue for both companies.
Ultimately, no one compound is likely to deliver a knockout punch to the pandemic coronavirus, in part because drug-resistant viruses are likely to emerge. Collins and others argue that the best strategy takes a page from the treatment for HIV and hepatitis C: mixing and matching antivirals aimed at several proteins, making it harder for the virus to evolve multiple workarounds at once. "We really need an arsenal," says Lillian Chiang, CEO of Evrys Bio, which is working on antivirals against host-cell proteins.
"This is going to take time," says Michael Sofia, a chief scientific officer with Arbutus Biopharma, a Canadian antiviral company. And money. According to recent estimates, bringing a new drug to market costs between $985 million and $2.8 billion. Anderson says Pfizer, for one, is committing company resources to defeating the pandemic without expectation of profit. Other companies say the same. But during previous lulls in infectious disease outbreaks, many drug companies abandoned work on antivirals. "As soon as this stops being a hot area, people will move on," Nwankwo says.
In another disincentive, antiviral treatments for SARS-CoV-2 might be given for only a week or two, giving drugmakers a narrow window to reap returns. As a result, Denison and others argue that more government support is needed to keep stocking the antiviral arsenal. Any lull in the battle against SARS-CoV-2 and its kin is likely to be temporary, they say.
"We are going to have another coronavirus," Mesecar says. "We just don't know what it will look like."
*Clarification, 11 March, 2:30 p.m.: This story has been updated to clarify a whistleblower's allegation.
.
Heliobas Disciple
TB Fanatic
/cloudfront-us-east-2.images.arcpublishing.com/reuters/5ZK7SN4K6RLSRNFVYCI7BAVQBU.jpg)
Moderna plots vaccines against 15 pathogens with future pandemic potential
Moderna Inc said on Monday it plans to develop and begin testing vaccines targeting 15 of the world's most worrisome pathogens by 2025 and will permanently wave its COVID-19 vaccine patents for shots intended for certain low- and middle-income countries.
www.reuters.com
Moderna plots vaccines against 15 pathogens with future pandemic potential
By Julie Steenhuysen and Michael Erman
March 7, 20227:29 PM ESTLast Updated 3 hours ago
March 7 (Reuters) - Moderna Inc (MRNA.O) said on Monday it plans to develop and begin testing vaccines targeting 15 of the world's most worrisome pathogens by 2025 and will permanently wave its COVID-19 vaccine patents for shots intended for certain low- and middle-income countries.
The U.S. biotechnology company also said it will make its messenger RNA (mRNA) technology available to researchers working on new vaccines for emerging and neglected diseases through a program called mRNA Access.
Moderna announced its strategy ahead of the Global Pandemic Preparedness Summit sponsored by the UK government and the Coalition for Epidemic Preparedness Innovations (CEPI), an international coalition set up five years ago to prepare for future disease threats.
Moderna is already collaborating with partners on vaccines against some of the 15 pathogens, which include Chikungunya, Crimean-Congo hemorrhagic fever, Dengue, Ebola, Malaria, Marburg, Lassa fever, MERS and COVID-19.
Those collaborations include a Nipah virus vaccine with the U.S. National Institutes of Health and an HIV vaccine with the Gates Foundation and the International AIDS Vaccine Initiative, Moderna President Stephen Hoge said in an interview.
The company will either seek out new partners for the others or develop them internally, he said.
Moderna Chief Executive Stephane Bancel told a virtual press briefing on Monday that the 15 viruses are known threats that have not been addressed by many large drugmakers. The COVID-19 pandemic, which has killed six million people worldwide and sickened millions more, has made clear that needs to change, Bancel said.
"Too many lives were lost in the last few years,” he said.
Early in the COVID pandemic, Moderna pledged not to enforce its vaccine patents during the emergency phase of the health crisis.
That has allowed for development of a vaccine manufacturing plant in Africa backed by the World Health Organization as part of a pilot project to give poor and middle-income countries the know-how to make COVID-19 vaccines.
Moderna said it will make that pledge permanent for the 92 low- and middle income countries that qualify for assistance under the COVAX Advance Market Commitment (AMC) led by the GAVI vaccine alliance.
A company spokesperson said Moderna will not enforce patents for COVID-19 vaccines developed in South Africa by WHO-backed Afrigen Biologics for AMC-92 low- and middle-income countries.
Although it will not enforce its patents in these countries, Hoge said Moderna does not intend to share its vaccine technology with the WHO-backed technology transfer hub in South Africa, in spite of lobbying efforts by the organization. read more
Earlier on Monday, the company said it will set up a manufacturing facility in Kenya, its first in Africa, to produce mRNA vaccines, including against COVID-19. read more
As part of its future pandemic plan, Moderna intends to make its technology available to academic research labs to test their own theories for vaccines to address emerging and neglected diseases. Hoge said some of these may eventually result in partnerships with Moderna to address the 15 priority pathogens.
"What we want to make sure happens is that scientists who have great ideas for how they could make vaccines will be able to access our standards and technology, almost as if they worked at Moderna," Hoge said.
Initially, the program will start with a few academic labs, but Hoge expects it to expand rapidly. He sees the program as a way to expand discovery of vaccines using mRNA technology.
"We want to make sure that we allow others to explore the space that frankly, we can't get to," he said. "And that's really what this is about."
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WHO contracts Deutsche Telekom to build global digital vaccine passport
“Corona has a grip on the world. Digitization keeps the world running. Digital vaccination certificates like the EU’s are key to this. We are pleased to be able to support
WHO contracts Deutsche Telekom to build global digital vaccine passport
“Corona has a grip on the world. Digitization keeps the world running. Digital vaccination certificates like the EU’s are key to this. We are pleased to be able to support the WHO in the fight against the pandemic,” said Al-Saleh.
By Amanda Brown
Published 5 days ago on March 2, 2022
The World Health Organization (WHO) has inked a contract with German telecommunication multinational corporation, Deutsch Telekom subsidiary T-Systems, to build the world’s first global vaccine passport system.
The WHO is partnering with German computing and network services company, T-Systems, and shared that the software system in development will enable global electronic verification of coronavirus vaccination certificates to deliver what amounts to a global vaccine passport.
The software model will be QR code-based and will be designed to enable authentication for other vaccine certificates such as yellow fever and polio. The WHO fully intends to provide support to its 194 member states to facilitate the implementation of the digital verification technology for countries’ national and regional verification of vaccine status.
“COVID-19 affects everyone. Countries will therefore only emerge from the pandemic together. Vaccination certificates that are tamper-proof and digitally verifiable build trust. WHO is therefore supporting member states in building national and regional trust networks and verification technology. The WHO’s gateway service also serves as a bridge between regional systems. It can also be used as part of future vaccination campaigns and home-based records,” said Garrett Mehl, unit head of the WHO’s Department of Digital Health and Innovation, on Deutsche Telekom’s website.
Adel Al-Saleh, member of the Deutsche Telekom AG Board of Management and CEO of T-Systems, explained health is a strategic growth area for T-Systems and digital certificates will play a key role in overcoming the challenges of the pandemic era as we venture deeper into the digital age.
“Corona has a grip on the world. Digitization keeps the world running. Digital vaccination certificates like the EU’s are key to this. We are pleased to be able to support the WHO in the fight against the pandemic. Health is a strategic growth area for T-Systems. Winning this contract underscores our commitment to the industry,” said Al-Saleh.
On the corporate website, T-Systems made a point of sharing WHO, in its partnership with the company, will build transparency and data protection into the system to satisfy issues about the privacy of medical data and how it will be used and monitored. It went on to explain that the ongoing development of the system will be open-source and will be accessible on the Github developer platform.
This isn’t T-System’s first rodeo. In 2021, they launched Europe’s first digital COVID-19 certificate that enabled travellers to prove their vaccination, test and recovery status on demand. The app’s QR code is stored locally on a user’s smart device and information such as name, date of birth and date of issue, as well as details of the vaccine or test will be contained in the digital certificate.
“When the certificates are checked, a digital signature located in the QR code is verified. T-Systems and SAP have developed a gateway on behalf of the European Commission, through which signature keys are exchanged between national back ends. This gateway is located in Luxembourg and hosted by the European Commission. In addition, the two companies have developed reference software and apps that the commission makes available to member states,” T-Systems said on its website about the European project.
Where regional and national digital vaccine passports are being abandoned, it appears the WHO digital passport is poised to take over and fill the gap.
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CDC warns travelers to avoid New Zealand, Thailand and Hong Kong due to 'very high' COVID levels
New Zealand, Thailand and Hong Kong were moved to the CDC’s level 4 risk category Monday due to "very high" COVID-19 levels.
www.usatoday.com
CDC warns travelers to avoid New Zealand, Thailand and Hong Kong due to 'very high' COVID levels
Bailey Schulz
03/07/22
Federal health officials are advising U.S. travelers to avoid New Zealand, Thailand and Hong Kong due to COVID-19.
The Centers for Disease Control and Prevention moved the three destinations to its level 4 COVID-19 risk category Monday due to their "very high" COVID-19 levels. The CDC advises all travelers, regardless of vaccination status, to avoid travel to level 4 destinations.
“If you must travel to these destinations, make sure you are fully vaccinated before travel,” the federal agency says on its website.
New Zealand and Thailand have eased entry requirements in recent weeks, while Hong Kong prohibits entry from outside Greater China among nonresidents.
The three join more than 130 other destinations on the CDC’s list of areas with “very high” rates of COVID-19.
Larger countries are considered to have very high COVID-19 levels when they report more than 500 new cases per 100,000 people over the past 28 days. Destinations with a population of 100,000 or fewer must report more than 500 cumulative new cases over the past 28 days.
Other changes to the CDC’s travel guidance on Monday include:
- Anguilla, Cape Verde, Fiji, Mexico, the Philippines and the United Arab Emirates moved from level 4 to level 3. The CDC says unvaccinated travelers should avoid nonessential travel to these areas.
- Angola, Djibouti, Ethiopia, Equatorial Guinea, the Gambia, Mauritania, Mozambique, Namibia and Senegal moved from level 3 to level 2. The CDC says unvaccinated travelers who are at an increased risk for severe illness from COVID-19 should avoid nonessential travel to these destinations.
- Niger moved from level 4 to level 1. The CDC says travelers should make sure they are fully vaccinated before traveling to level 1 destinations.
- The Republic of the Congo, Cote d’Ivoire, Kenya, Lesotho, Rwanda, Togo and Uganda moved from level 2 to level 1.
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As virus cases go from 1 to 24,000, New Zealand changes tack
Back in August, New Zealand’s government put the entire nation on lockdown after a single community case of the coronavirus was detected
abcnews.go.com
As virus cases go from 1 to 24,000, New Zealand changes tack
Back in August, New Zealand’s government put the entire nation on lockdown after a single community case of the coronavirus was detected
By NICK PERRY Associated Press
March 8, 2022, 12:44 AM
WELLINGTON, New Zealand -- Back in August, New Zealand's government put the entire nation on lockdown after a single community case of the coronavirus was detected.
On Tuesday, when new daily cases hit a record of nearly 24,000, officials told hospital workers they could help out on understaffed COVID-19 wards even if they were mildly sick themselves.
It was the latest sign of just how radically New Zealand's approach to the virus has shifted, moving from elimination to suppression and now to something approaching acceptance as the omicron variant has taken hold.
Experts say New Zealand's sometimes counterintuitive actions have likely saved thousands of lives by allowing the nation to mostly avoid earlier, more deadly variants and buying time to get people vaccinated. The nation of 5 million has reported just 65 virus deaths since the pandemic began.
But virus hospitalizations have been rapidly rising, hitting a record of more than 750 on Tuesday and putting strain on the system.
Across the country, the explosion in cases has left people stunned. Just a month ago, case numbers were around 200 per day. Now, the outbreak is affecting everyone from frontline workers to lawmakers.
Opposition Leader Christopher Luxon became the highest profile politician yet to announce he was infected on Monday, saying he felt fine and would continue working from home.
One factor that hastened the outbreak was the return of thousands of university students to campuses around the country last month.
Ralph Zambrano, the student president at Victoria University of Wellington, said the virus had spread rapidly through hundreds of students in residence halls, taking a toll on their mental health and well-being.
“The campus would usually be buzzing at this time of year but it has a very eerie feeling to it,” he said, adding that most students were opting to learn remotely. “There's lots of anxiety and tension.”
He said the outbreak had strained the food supply system in the halls, with some students being offered only a protein drink for breakfast or a piece of cold meat and some peas for dinner.
The university said case numbers in the halls were now reducing as students recovered.
Professor Michael Baker, an epidemiologist at the University of Otago, said the variant had proved as ferociously infectious in New Zealand as it had in other countries.
He said cases appeared to be plateauing or even starting to dip in the largest city of Auckland, while still rising elsewhere.
While much of the world was breathing a sigh of relief after two years of terrible problems, Baker said, New Zealand was at its worst point yet in the pandemic and was coming to terms with the fact the virus would remain in the country permanently.
He said he was concerned health authorities had lost the ability to properly track the outbreak, as they struggled to shift from a system where they carefully monitored a few cases to dealing with thousands of self-reported results from rapid antigen tests.
Dr. Caroline McElnay, the director of public health at the Ministry of Health, told reporters the number of hospitalizations would grow, but that patients with omicron generally had less severe illnesses than previous patients had experienced with the delta variant.
She said the rising number of both patients and infected health workers had prompted the relaxation in the rules around when health workers could return to hospitals.
She said infected workers would only be allowed to work with patients who already had the virus, and if there were no other options.
“It's an extra tool that enables our health system to keep running,” she said.
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Review, infections and complications
28 min 12 sec
Mar 7, 2022
Dr. John Campbell
Avoidable mortality rates at highest level since 2010 In 2020, 22.8% of all deaths in Great Britain (GB) were considered avoidable. This figure represents about 153,000 of the total 672,000 deaths. Long COVID and mental disorders in school age Primary age with long covid 30.0% had a probable mental disorder Primary age without long covid 7.7.0% had a probable mental disorder Primary aged 1% have experienced long covid Secondary school age with long covid 22.6% had a probable mental disorder Secondary school age without long covid 13.6% had a probable mental disorder Secondary aged 2.7% have experienced long covid UK prevalence, week to end of February 1,933,500 people (1 in 30) in England 94,200 people (1 in 30) in Wales 106,300 people (1 in 17) in Northern Ireland 280,500 people (1 in 19) in Scotland Deaths involving COVID-19 continue to fall Week ending 18 February 2022 969 deaths in the week 217 fewer than the previous week Total deaths in the week, 12,742, 6.4% below the five-year average Of the 863 deaths registered (where covid was mentioned), 64.8% (559 deaths) recorded as the underlying cause of death Presence of antibodies previously had COVID-19 infection or been vaccinated Week beginning 31 January 2022 98.2% in England 97.9% in Wales 98.2% in Northern Ireland 98.2% in Scotland Long COVID have had it for at least a year As of the end of January 2022 1.5 million people (2.4%) living with long COVID (over 4 weeks) 685,000 (45%) symptoms at least a year 65% (989,000) of those with self-reported long COVID, it affected their day-to-day activities Fatigue, 51% Prevalence aged 35 to 49 years, females, people living in more deprived areas, working in teaching and education, social care or healthcare, those with another activity-limiting health condition or disability
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American Lockdowns Began Two Years Ago Today ⋆ Brownstone Institute
Certain dates should live in infamy. One is March 7, 2020. That is the date that the American lockdowns began in Austin, TX
brownstone.org
American Lockdowns Began Two Years Ago Today
By Jeffrey A. Tucker
March 7, 2022
Certain dates should live in infamy. One is March 7, 2020. That is the date that the Austin, Texas, Mayor, Steve Adler, acting on his own at least in public, canceled the in-person conference South By Southwest (possibly attracting as many as a quarter million people) that was set to begin in the city five days later.
There were zero cases in Austin at the time. Later, he along with most mayors and governors, imposed stay-at-home orders, imposed curfews, and eventually shut bars and restaurants.
The cancellation did not stop the virus from coming to Austin. In November, while Adler was ordering citizens to stay home and stay safe, and Austin was by then flooded with cases, he and 20 friends boarded a private plane to Cabo San Lucas in Baja, California, and had a glorious time. He even made a video while vacationing that brazenly ordered citizens to do what he was not doing.
The Austin-American Statesman reported:
In early November, as health officials warned of an impending COVID-19 spike, Austin Mayor Steve Adler hosted an outdoor wedding and reception with 20 guests for his daughter at a trendy hotel near downtown.
The next morning, Adler and seven other wedding attendees boarded a private jet bound for Cabo San Lucas, Mexico, where they vacationed for a week at a family timeshare.
One night into the trip, Adler addressed Austin residents in a Facebook video: “We need to stay home if you can. This is not the time to relax. We are going to be looking really closely. … We may have to close things down if we are not careful.”
Once found out, he apologized for misjudgement.
So far as I know, this was the first instance of American lockdown. Thus began the executive decision making, the compulsion, the unscientific overreaction, the hypocrisy, and the age of calamity in which we’ve lived for two years.
On that day, I had expected massive protests from all tech companies, artists, the hospitality industry, and airlines. I figured that left, right, and center would all unite and decry this decision as a flat-out violation of American liberties and property rights. We are not China. We have a Bill of Rights. Instead, there was near silence. I simply could not believe it.
At the time, I wrote: “Based on the Austin, Texas, precedent, any mayor of any town in America can right now declare a state of emergency, cancel events, shut malls, and close parks. Who is to stop them from shuttering stores, restaurants, schools, and churches, and quarantining whole neighborhoods?”
Below I reprint the column I wrote on March 8, 2020. The reaction to my column was floods of outrage that I could have imagined this conference going ahead in the midst of a dangerous pandemic. We know now that 1) the demographics of danger did not affect what would have been the typical attendee of the event, 2) the presence of international travel made no difference since the virus was here anyway, and 3) such cancellations at best only delayed the time at which endemicity would have arrived due to exposure and recovery. I maintain to this day that the conference should have gone ahead.
The following year, the conference took place entirely online, which is to say that it did not really take place at all.
Here is my original column as written:
Imagine if you are the organizer of a major arts and tech event that attracts a quarter-million attendees. One week out from the conference, the mayor cancels your event. Your event is not named specifically, just that all events involving more than 2,500 people are officially banned. He does this using emergency powers, justified in the name of containing a virus.
And that’s it. This is what happened to South by Southwest, one of the most important events in the world in Austin, Texas, which has thus far not reported a single case of COVID-19. Based on last year’s numbers, It’s the end for:
- 73,716 conference attendees and 232,258 festival attendees;4,700 speakers
- 4,331 media/press attendees
- 2,124 sessions
- 70,00 trade show attendees occupying 181,400 square feet of exhibit space
- 351 official parties and events
- 612 international acts
- 1,964 performance acts
Draconian, to say the least.
Making matters worse, a vicious and completely false report published by Variety said that the festival was aching for the city to make the call so that the festival could collect insurance money. This turns out to be entirely wrong: South by Southwest had no insurance against infectious disease. It was a smear and response to mass frenzy. After all, a petition on Change.org signed by 55,000 people had demanded the cancellation.
The city acquiesced to the mob. A grand and glorious conference was destroyed – the first of many this season.
Italy now has 16 million people under quarantine, which is to say that they are prisoners.
Anyone living in Lombardy and 14 other central and northern provinces will need special permission to travel. Milan and Venice are both affected. Prime Minister Giuseppe Conte also announced the closure of schools, gyms, museums,
nightclubs and other venues across the whole country. The measures, the most radical taken outside China, will last until 3 April.
Americans have been quarantined on cruise ships and then forced to pay for their later hospitalization. The government that quarantines you has zero intention to pay the costs associated with your care, to say nothing of the opportunity costs of missing work.
The press isn’t helping. The New York Times has cheered it all on, aggressively advocating that governments go Medieval on this one.
In six months, if we are in a recession, unemployment is up, financial markets are wrecked, and people are locked in their homes, we’ll wonder why the heck governments chose disease “containment” over disease mitigation. Then the conspiracy theorists get to work.
The containment strategy was never debated or discussed. For the first time in modern history, governments of the world have taken it upon themselves to control population flows in the hopes of stemming the spread of this disease – regardless of the cost and with scant evidence that this strategy will actually work.
More and more, the containment response is looking like global panic. What’s interesting, Psychology Today points out, is that your doctor is not panicking:
COVID-19 is a new virus in a well-known class of viruses. The coronaviruses are cold viruses. I’ve treated countless patients with coronaviruses over the years. In fact, we’ve been able to test for them on our respiratory panels for the entirety of my career.
We know how cold viruses work: They cause runny noses, sneezing, cough, and fever, and make us feel tired and achy. For almost all of us, they run their course without medication. And in the vulnerable, they can trigger a more severe illness like asthma or pneumonia.
Yes, this virus is different and worse than other coronaviruses, but it still looks very familiar. We know more about it than we don’t know.
Doctors know what to do with respiratory viruses. As a pediatrician, I take care of patients with hundreds of different viruses that behave similarly to this one. We take care of the kids at home and see them if the fever is prolonged, if they get dehydrated, or if they develop breathing difficulty. Then we treat those problems and support the child until they get better.
Meanwhile, the New England Journal of Medicine reports as follows:
On the basis of a case definition requiring a diagnosis of pneumonia, the currently reported case fatality rate is approximately 2%. In another article in the Journal, Guan et al. report mortality of 1.4% among 1,099 patients with laboratory-confirmed Covid-19; these patients had a wide spectrum of disease severity. If one assumes that the number of asymptomatic or minimally symptomatic cases is several times as high as the number of reported cases, the case fatality rate may be considerably less than 1%. This suggests that the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza (which has a case fatality rate of approximately 0.1%) or a pandemic influenza (similar to those in 1957 and 1968) rather than a disease similar to SARS or MERS, which have had case fatality rates of 9 to 10% and 36%, respectively.
Slate’s piece on this topic offers more perspective:This all suggests that COVID-19 is a relatively benign disease for most young people, and a potentially devastating one for the old and chronically ill, albeit not nearly as risky as reported. Given the low mortality rate among younger patients with coronavirus—zero in children 10 or younger among hundreds of cases in China, and 0.2-0.4 percent in most healthy nongeriatric adults (and this is still before accounting for what is likely to be a high number of undetected asymptomatic cases)—we need to divert our focus away from worrying about preventing systemic spread among healthy people—which is likely either inevitable, or out of our control—and commit most if not all of our resources toward protecting those truly at risk of developing critical illness and even death: everyone over 70, and people who are already at higher risk from this kind of virus.
Look, I’m obviously not in a position to comment on the medical aspects of this; I defer to the experts. But neither are medical professionals in a position to comment on the political response to this; mostly they have assiduously declined to do so.
Meanwhile, governments are willy-nilly making drastic decisions that profoundly affect the status of human freedom. Their decisions are going to affect our lives in profound ways. And there has thus far been no real debate on this. It’s just been presumed that containment of the spread rather than the care of the sick is the only way forward.
What’s more, we have governments all-too-willing to deploy their awesome powers to control human populations in direct response to mass public pressure based on fears that have so far not been justified by any available evidence.
Based on the Austin, Texas, precedent, any mayor of any town in America can right now declare a state of emergency, cancel events, shut malls, and close parks. Who is to stop them from shuttering stores, restaurants, schools, and churches, and quarantining whole neighborhoods?
For this reason, we have every reason to be concerned.
Are we really ready to imprison the world, wreck financial markets, destroy countless jobs, and massively disrupt life as we know it, all to forestall some uncertain fate, even as medical professionals do know the right way to deal with respiratory illness in general from a medical point of view? It’s at least worth debating.
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People With Heart Defects at Greater Risk for Severe COVID-19 Illness and Death
People with congenital heart defects who were hospitalized with COVID-19 were up to twice as likely to suffer severe illness or death from the virus compared to people who were not born with a heart defect, according to a new study. People with a heart defect plus another underlying medical condi
scitechdaily.com
People With Heart Defects at Greater Risk for Severe COVID-19 Illness and Death
By American Heart Association
March 7, 2022
- People with congenital heart defects who were hospitalized with COVID-19 were up to twice as likely to suffer severe illness or death from the virus compared to people who were not born with a heart defect, according to a new study.
- People with a heart defect plus another underlying medical condition, including heart failure, pulmonary hypertension, Down syndrome, diabetes, or obesity, were among those most at risk of having severe COVID-19 illness.
Among those at the highest risk for the most severe COVID-19 illness were patients who had a heart defect and another health condition, were ages 50 and older, or were men, according to the study.
There are more than a dozen types of congenital heart defects, which result when the heart, or blood vessels near the heart don’t develop normally before birth. According to the American Heart Association’s Heart Disease and Stroke Statistics—2022 Update, congenital heart defects are the most common birth defect worldwide, with a global prevalence of 157 per 100,000 in 2017.
“Data comparing COVID-19 outcomes among individuals with and without congenital heart defects has been limited,” said lead author Karrie Downing, M.P.H., an epidemiologist at the National Center on Birth Defects and Developmental Disabilities and the COVID-19 Response Team at the U.S. Centers for Disease Control and Prevention in Atlanta.
Researchers examined data on hospitalized COVID-19 patients from March 2020 to January 2021, collected in the Premier Healthcare Database Special COVID-19 Release, a database representing approximately 20% of all U.S. hospitalizations. The COVID-19 patients with and without heart defects in this study received care in the same hospitals. Differences in age, gender, race/ethnicity, health insurance types and other high-risk conditions (specifically heart failure, pulmonary hypertension, Down syndrome, diabetes, and obesity) were accounted for across those populations.
During this period, the database had more than 235,000 patients, ages 1 to 64 years old, who were hospitalized for COVID-19. Patients were divided into two groups: those who had a congenital heart defect and those who did not. Across these two categories, researchers then determined how many required an admission to the ICU, needed a ventilator to help with breathing or died. Researchers also reviewed other characteristics including other health conditions.
Of the 235,638 hospitalized COVID-19 patients evaluated for this study, 421 or 0.2% had a congenital heart defect. The analysis found:
- among the patients with a heart defect, most were over the age of 30 (73%), and 61% were male; 55% were non-Hispanic white people, 19% were Hispanic people and 16% were non-Hispanic Black people;
- overall, 68% of the patients with a heart defect also had at least one other health condition noted, compared to 59% among those without a congenital heart defect;
- 54% of patients with a congenital heart defect were admitted to the ICU compared to 43% of those without a congenital heart defect;
- 24% of patients with a congenital heart defect required a ventilator to breathe compared to 15% of those without a congenital heart defect; and
- 11% of patients with a congenital heart defect died during hospitalization compared to 7% of those without a congenital heart defect.
In addition, people with congenital heart defects consistently remained at high-risk for severe COVID-19 illness, even when divided into categories by age or other health conditions noted in the study, according to the researchers.
Downing believes these findings have immediate, practical relevance for health care professionals as the COVID-19 pandemic continues to evolve: “People with heart defects should be encouraged to receive the COVID-19 vaccines and boosters and to continue to practice additional preventive measures for COVID-19, such as mask-wearing and physical distancing. People with heart defects should also consult with their health care teams about additional steps to manage personal risks related to COVID-19, given the significantly increased risk of severe infection and serious complications.”
Downing noted that not all patients with heart defects who were hospitalized with COVID-19 had poor outcomes. “More work is needed to identify why the clinical course of COVID-19 disease results in significantly worse outcomes for some hospitalized patients with risk factors for critical COVID-19 illness, like heart defects, and not for others,” she said.
There are several limitations to this study. Only people already hospitalized with COVID-19 were included, the clinical details about the underlying heart defect were not available, and lab testing to identify and/or confirm COVID-19 diagnoses may vary by hospital. Lastly, COVID-19 vaccination status was not considered, since the vaccines became available in the U.S. starting in December 2020.
Reference: 7 March 2022, Circulation.
DOI: 10.1161/CIRCULATIONAHA.121.057833
Co-authors are Regina Simeone, Ph.D.; Matthew Oster, M.D., M.P.H.; and Sherry Farr, Ph.D. Authors’ disclosures are listed in the manuscript.
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Covid can cause regions of the brain to SHRINK
Brain scans from people who have been infected with Covid have revealed tissue damage and shrinking in regions of the brain linked to smell.
'Covid brain' IS real: Illness can cause regions of the brain to SHRINK and lead to cognitive decline, new study finds
By Bhvishya Patel
Published: 21:16 EST, 7 March 2022 | Updated: 21:37 EST, 7 March 2022
- Scientists looked at MRI scans from people who have been infected with Covid
- Revealed tissue damage and shrinking in regions of the brain linked to smell
- Examined the brains of 785 participants aged 51-81 who had received scans
- The findings from the latest study have been published in the journal Nature
Brain scans from people who have been infected with Covid-19 have revealed tissue damage and shrinking in regions of the brain linked to smell, according to researchers.
During their study scientists from the University of Oxford examined the brains of 785 participants aged 51-81 who had received MRI scans both before and after infection.
A total of 401 participants tested positive for infection with Sars-CoV-2 between their two scans, of whom 15 were admitted to hospital.
According to scientists, brain scans revealed the effects of the virus included a greater reduction in grey matter thickness in the regions of the brain which are associated with smell and the memory of events.
Participants who had Covid-19 also displayed evidence of tissue damage in regions of the brain linked to smell, and an average reduction in whole brain sizes.
On average, the participants who were infected with SARS-CoV-2 also showed greater cognitive decline between their two scans, associated with the atrophy of a brain region known as the cerebellum, which is linked to cognition.
The findings from the study, which were published in the journal Nature, now provide evidence of changes to the human brain following a Covid-19 infection and the emergence of 'Covid brain'.
However it is not yet clear whether the cognitive decline can be reversed over time.
Dr Max Taquet, NIHR Oxford Health BRC senior research fellow at the University of Oxford, said: 'This is the first large-scale study to investigate the actual changes in the brain that can occur after a Covid-19 infection.
'It is well established that Covid-19 infection is associated with subsequent risks of neurological and psychiatric problems in some people including brain fog, loss of taste and smell, depression, and psychosis.
'But why this occurs remains largely unknown. This study starts to shed light on this important question by showing that brain regions connected to the 'smell centre' of the brain can shrink after Covid-19 in some people.
'These brain changes were not observed in every patients and they were mostly subtle.
'These findings might help explain why some people experience brain symptoms long after the acute infection.
'The causes of these brain changes, whether they can be prevented or even reverted, as well as whether similar changes are observed in hospitalised patients, in children and younger adults, and in minority ethnic groups, remain to be determined.'
The study looked at those who had received brain scans before and during the pandemic as part of the UK Biobank study - a large database that includes genetic and health information on half-a-million people living in the UK.
The authors identified various long-term effects following infection - with an average of 141 days between participants receiving a Covid diagnosis and the second imaging scan.
The latest research comes after scientists at the University of Edinburgh uncovered more than a dozen genetic quirks that may explain why some people are more vulnerable to severe Covid than others.
Up to 16 changes to DNA were found in patients critically ill with the virus, many of which are involved in blood clotting and inflammation.
One genetic variant was found to be slower at signalling to the immune system that cells were under attack from the virus.
Having just one of the genes could be the difference between getting a cough or being admitted to intensive care, according to the biggest study of its kind.
As part of the Government-funded research, experts at the University of Edinburgh studied the genes of more than 57,000 people across the UK, including 9,000 Covid patients.
The study, partly funded by the Department of Health, did not break down the risk of becoming severely ill per gene, or which Britons might be more at risk then others based on their heritage.
However, they said some genes were linked to a doubling of the risk of severe illness from Covid.
This is not the first time studies have found different genes could predispose certain people to becoming severely ill with Covid.
But the scientists hope the latest finding will help identify new drugs and treatments in the future.
Yesterday figures showed that Britain had recorded 126,605 Covid cases over the last three days.
Government dashboard data revealed the combined infections on Saturday, Sunday and Monday were 54 per cent higher than the total last week.
Some 42,000 cases were spotted over the past three days, on average, up from 27,400 a week ago.
Officials have stopped releasing the daily figures at weekends as part of a wind-down of the way the pandemic is reported, meaning a three-day total is released every Monday.
Another 139 Covid fatalities were registered over the weekend, up by one on the 138 last week.
Meanwhile, latest hospital data showed 1,287 admissions were recorded on March 1, up 15 per cent on the tally from a week ago.
The flare-up in infections comes after England's 'Freedom Day' on February 24 and amid the spread of a more infectious version of Omicron.
BA.2 was behind 52 per cent of all Covid infections in the seven days to February 20, the UK Health Security Agency found.
The sub-variant has completed its rapid rise to dominance just a month after it was first spotted in the UK.
But the scientific community has said there is no reason to panic, with the variant already almost every case in Denmark but leading to no effect on hospitalisations or deaths.
Experts warn the more infectious variant may cause some fluctuations in case rates, but say there is no evidence the strain is more likely to cause severe disease.
Yesterday national clinical director for Scotland Professor Jason Leitch told BBC Radio Scotland's Good Morning Scotland there was no reason to 'panic' over rising cases.
'I'm not panicking – I'm not thinking we should suddenly go back to restrictions or protections, but I am concerned,' he said.
'As we mix more, the virus gets more opportunities, so we've got 10,000 cases a day, we've had a little bit of an increase in those in hospital – it's not huge, so people shouldn't panic, but this disease is not over and it's not done with us.'
He stressed the importance of vaccine uptake to allow for the continued suppression of the virus.
'You should still be cautious, particularly around those who are vulnerable,' he said.
'So get your vaccine, particularly if you're getting a letter now if you're in one of these elderly groups, or vulnerable groups.
'Test – because that testing is still available – and follow the guidance.'
Last month the government ended its Covid laws that it had introduced to tackle the pandemic.
Boris Johnson said England was exiting the 'grimmest years in our peacetime' as he unveiled his 'Living With Covid' strategy.
And health secretary Sajid Javid described how the day would go down in the history books — as an 'important' next step in a new phase of the pandemic.
But he urged people to remain 'sensible' in the next stage of the country's battle with Covid, warning that the virus 'is not done with us' with new and challenging variants expected to emerge.
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medicalxpress.com
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How COVID-19 can change the brain
March 7, 2022
Scientists have discovered that even a mild case of COVID-19 might inflict damage on your brain.
On average, middle-aged and older adults who'd been sick with COVID showed signs of tissue shrinkage in brain areas related to the sense of smell, the researchers reported. They also tended to have more trouble completing complex mental tasks, when compared to people with no history of COVID-19—an effect that was most striking among the oldest adults.
Experts said the findings strengthen evidence that even mild COVID-19 may cause detectable deficits in the brain.
That's because the researchers had access to brain scans taken from people both before and after they'd been infected. That helps distinguish brain changes associated with COVID-19 from any abnormalities that may have already been there.
"We still cannot be sure with 100% certainty that there is a causal effect of the infection," said lead researcher Gwenaelle Douaud, a professor at the University of Oxford, in the United Kingdom.
"But," she added, "we can disentangle the effects that we observe from differences that may have pre-existed in the brain of the participants before they became infected with SARS-CoV-2."
There are still key questions, however. What caused the brain changes? And what, precisely, do they mean?
Recent research has estimated that up to 30% of people with COVID-19 develop "long-haul" symptoms that plague them well after they've beaten the infection. The list includes fatigue, headaches, shortness of breath, dulled sense of smell and taste, and problems with memory and concentration that have been dubbed "brain fog."
Experts still do not know what causes "long COVID," or why it can strike after a mild infection. One theory pins the blame on overactivation of the immune system, leading to widespread inflammation in the body.
Dr. Joanna Hellmuth is a neurologist at the University of California, San Francisco, who is studying post-COVID symptoms. She said it's not clear what may have caused the brain changes seen in this study.
But Hellmuth said the fact that tissue shrinkage occurred in smell-related areas points to one possibility: lack of sensory input. Particularly during the pandemic's early waves, COVID-19 commonly caused people to lose their sense of smell.
Hellmuth cautioned against seeing alarm in the findings. She noted that the average brain changes were "small," and do not mean that people with mild COVID-19 face the prospect of brain "degeneration."
The study, published online March 7 in the journal Nature, included 785 British adults aged 51 to 81. All had undergone brain scans before the pandemic, as part of a research project called the UK Biobank. They came back for a second scan during the pandemic.
In that group, 401 contracted COVID-19 at some point between the two brain scans, while 384 did not. Nearly all who fell ill—96%—had a milder case. The second scan was taken an average of 4.5 months after their illness.
On average, Douaud's team said, the COVID group showed greater tissue loss in specific brain areas related to smell, plus a bigger reduction in overall brain size.
The effect amounted to an extra 0.2% to 2% tissue loss, the investigators found.
Douaud agreed that a lack of sensory input might explain the changes in smell-related brain areas. But, she said, her team did not know whether participants had, in fact, lost their sense of smell. So they could not look for correlations between those symptoms and brain changes.
The researchers were able to look at participants' performance on some standard tests of mental sharpness. And again, the COVID-19 group showed a greater decline, on average.
The divide was most clear among the oldest adults, Douaud said: People in their 70s who'd had COVID worsened by 30%, on average. That compared with 5% among their COVID-free peers.
There was some evidence that performance decline correlated with shrinkage in a brain structure involved in thinking and other mental skills.
It is possible, Douaud said, that the brain changes associated with COVID-19 resolve over time.
"The best way to find out would be to scan these participants again in one or two years' time," she said.
Another question is whether the results apply to people who've had COVID-19 in more recent times. The study participants were infected earlier in the pandemic, before the rise of the Delta, and then Omicron, variants, the researchers noted.
Plus, Hellmuth said, now there are vaccines, and recent studies suggest vaccination curbs the chances of developing long COVID. It's not clear from this study how vaccination might influence brain changes.
Explore further People with certain genetic loci are 11% more likely to lose the ability to smell or taste from COVID .
www.nature.com
How COVID-19 can change the brain
Scientists have discovered that even a mild case of COVID-19 might inflict damage on your brain.
How COVID-19 can change the brain
March 7, 2022
Scientists have discovered that even a mild case of COVID-19 might inflict damage on your brain.
On average, middle-aged and older adults who'd been sick with COVID showed signs of tissue shrinkage in brain areas related to the sense of smell, the researchers reported. They also tended to have more trouble completing complex mental tasks, when compared to people with no history of COVID-19—an effect that was most striking among the oldest adults.
Experts said the findings strengthen evidence that even mild COVID-19 may cause detectable deficits in the brain.
That's because the researchers had access to brain scans taken from people both before and after they'd been infected. That helps distinguish brain changes associated with COVID-19 from any abnormalities that may have already been there.
"We still cannot be sure with 100% certainty that there is a causal effect of the infection," said lead researcher Gwenaelle Douaud, a professor at the University of Oxford, in the United Kingdom.
"But," she added, "we can disentangle the effects that we observe from differences that may have pre-existed in the brain of the participants before they became infected with SARS-CoV-2."
There are still key questions, however. What caused the brain changes? And what, precisely, do they mean?
Recent research has estimated that up to 30% of people with COVID-19 develop "long-haul" symptoms that plague them well after they've beaten the infection. The list includes fatigue, headaches, shortness of breath, dulled sense of smell and taste, and problems with memory and concentration that have been dubbed "brain fog."
Experts still do not know what causes "long COVID," or why it can strike after a mild infection. One theory pins the blame on overactivation of the immune system, leading to widespread inflammation in the body.
Dr. Joanna Hellmuth is a neurologist at the University of California, San Francisco, who is studying post-COVID symptoms. She said it's not clear what may have caused the brain changes seen in this study.
But Hellmuth said the fact that tissue shrinkage occurred in smell-related areas points to one possibility: lack of sensory input. Particularly during the pandemic's early waves, COVID-19 commonly caused people to lose their sense of smell.
Hellmuth cautioned against seeing alarm in the findings. She noted that the average brain changes were "small," and do not mean that people with mild COVID-19 face the prospect of brain "degeneration."
The study, published online March 7 in the journal Nature, included 785 British adults aged 51 to 81. All had undergone brain scans before the pandemic, as part of a research project called the UK Biobank. They came back for a second scan during the pandemic.
In that group, 401 contracted COVID-19 at some point between the two brain scans, while 384 did not. Nearly all who fell ill—96%—had a milder case. The second scan was taken an average of 4.5 months after their illness.
On average, Douaud's team said, the COVID group showed greater tissue loss in specific brain areas related to smell, plus a bigger reduction in overall brain size.
The effect amounted to an extra 0.2% to 2% tissue loss, the investigators found.
Douaud agreed that a lack of sensory input might explain the changes in smell-related brain areas. But, she said, her team did not know whether participants had, in fact, lost their sense of smell. So they could not look for correlations between those symptoms and brain changes.
The researchers were able to look at participants' performance on some standard tests of mental sharpness. And again, the COVID-19 group showed a greater decline, on average.
The divide was most clear among the oldest adults, Douaud said: People in their 70s who'd had COVID worsened by 30%, on average. That compared with 5% among their COVID-free peers.
There was some evidence that performance decline correlated with shrinkage in a brain structure involved in thinking and other mental skills.
It is possible, Douaud said, that the brain changes associated with COVID-19 resolve over time.
"The best way to find out would be to scan these participants again in one or two years' time," she said.
Another question is whether the results apply to people who've had COVID-19 in more recent times. The study participants were infected earlier in the pandemic, before the rise of the Delta, and then Omicron, variants, the researchers noted.
Plus, Hellmuth said, now there are vaccines, and recent studies suggest vaccination curbs the chances of developing long COVID. It's not clear from this study how vaccination might influence brain changes.
Explore further People with certain genetic loci are 11% more likely to lose the ability to smell or taste from COVID .
SARS-CoV-2 is associated with changes in brain structure in UK Biobank - Nature
After infection with SARS-CoV-2, individuals show a greater reduction in grey matter thickness and tissue contrast in the orbitofrontal cortex and parahippocampal gyrus; greater changes in markers of tissue damage in regions that are functionally connected to the primary olfactory cortex; and a...
www.nature.com
Heliobas Disciple
TB Fanatic
I am posting this because it's from the Lancet, as mainstream as you can get for 'medical news'. This is a news thread, so I'm posting what this reputable publication is telling the population that looks to them for medical news.
medicalxpress.com
(fair use applies)
Large US study confirms most mRNA COVID-19 vaccine side effects are mild and temporary
by Lancet
March 7, 2022
A review of adverse events following vaccination against COVID-19 with mRNA vaccines in the U.S. confirms that most side effects were mild and decreased substantially after one day. The new study, published in The Lancet Infectious Diseases journal, suggests that for more than 298 million vaccine doses administered between December 2020 and June 2021, 92% (313,499/340,522) of reported adverse events were not serious, and less than 1% of v-safe participants reported seeking any medical care following vaccination.
In December 2020 two mRNA COVID-19 vaccines—Pfizer-BioNTech (BNT162b2) and Moderna (mRNA-1723) – were authorised for emergency use in the U.S.. Both vaccines involved two primary doses and have shown good safety profiles in clinical trials, with mild effects such as injection site pain, fatigue, and headache being reported as the most common adverse events.
As is the case for all vaccines in the U.S., anyone can report adverse events using the Vaccine Adverse Event Reporting System (VAERS), a long-standing reporting system run jointly by US Centers for Disease Control and Prevention (CDC) and the US Food and Drug Administration (FDA). With VAERS, US residents, their healthcare providers, or vaccine manufacturers can submit any event experienced following receipt of a vaccine. These reports are categorised as non-serious, serious, or death. The v-safe system, managed by CDC, was developed specifically for the COVID-19 vaccination programme, and consists of smartphone-based surveys sent daily for the first week after vaccination (and at longer time intervals in the months following) to monitor adverse reactions.
"Vaccines are the most effective tool to prevent serious COVID-19 disease outcomes and the benefits of immunisation in preventing serious illness and death strongly favour vaccination," says study author, Dr. Hannah Rosenblum, U.S. Centers for Disease Control and Prevention (CDC). "COVID-19 vaccine safety monitoring is the most robust in US history and the two complementary surveillance systems used in this study should bolster confidence that mRNA COVID-19 vaccines are safe."
This study looked at available VAERS and v-safe self-reported data between December 2020 and June 2021 following both doses of either the Pfizer-BioNTech or Moderna mRNA vaccines. During the study period, over 298 million doses of mRNA vaccines were administered (132 million Moderna and 167 million Pfizer).
VAERS received over 340,000 reports of adverse effects with more than 313,000 (92%) registered as non-serious, including headache (64,064/340,522 or 20%), fatigue (52,048/340,522 or 17%), fever (51,023/340,522 or 16%), chills (49,234/340,522 or 16%) and pain (47,745/340,522 or 15%). Of the more than 22,000 (6.6%) side effects registered as serious, the most common was shortness of breath (4,175/340,522 or 15%). Of 340,522 adverse events reported to VAERS during the study period, approximately 4500 (1.3%) were deaths, with more than 80% of these deaths among people ages 60 years or older. Because COVID-19 vaccines have been authorised under emergency use, healthcare providers are required to report all deaths following vaccination, regardless of the potential direct association. The study authors note that no unusual patterns were detected in cause death reports.
"The rapid pace at which COVID-19 vaccines were administered under emergency use, especially among older populations, was unprecedented. Due to their age, this group already has a higher baseline mortality rate than the general population and our results follow similar patterns of deaths rates for people in this age group following other adult vaccinations," says study author Dr. David Shay, also of the CDC.
Of the nearly 8 million v-safe participants, over half reported local (4.6 million) and systemic (3.6 million) reactions post-vaccination, occurring more frequently after dose two than dose one. Side effects were most frequently reported the day after vaccination and were nearly all mild, with the most common being fatigue (2,295,205/6,775,515 or 34% after dose one, 3,158,229/5,674,420 or 56% after dose two), headache (1,831,471/6,775,515 or 27% after dose one, 2,623,721/5,674,420 or 46% after dose two), and injection site pain (4,488,402/6,775,515 or 66% after dose one, 3,890,848/5,674,420 or 69% after dose two).
More v-safe reports of being unable to work, perform normal activities, or seeking medical care were reported after dose two (1,821,421/5,674,420 or 32%), than after dose one (808,963/6,775,515 or 12%). Less than 1% of participants (56,647 after dose one and 53,077 after dose two) reported seeking medical care after either vaccine dose.
Study author Dr. Tom Shimabukuro (US CDC) says: "VAERS and v-safe are important tools CDC can use when evaluating vaccine safety and to help identify any unexpected or unusual events. These data are reassuring that reactions to both mRNA vaccines are generally mild and subside after one or two days—confirming reports from clinical trials and post-authorization monitoring."
The authors acknowledge some limitations with this research. Firstly, the VAERS system relies on spontaneous reporting and is not representative of the entire population. This also means that while it can monitor for potential safety signals, it cannot define a causal relationship between vaccination and adverse events. This limitation lies with the surveillance system and not the study design. In addition, the need for smartphone access to participate in v-safe excludes populations without access to these devices. Finally, although trends in differences in adverse reactions have emerged among the Pfizer-BioNTech and Moderna mRNA vaccines, neither VAERS nor v-safe can definitively measure the safety differences between the two vaccines.
Writing in a linked comment, Elizabeth Phillips, Vanderbilt University Medical Center U.S., who was not involved in the study, said: "Reassuringly, the six-month VAERS data supports that, although approximately one in 1,000 individuals vaccinated may have an adverse effect, most of these are non-serious. No unusual patterns emerged in the cause of death or serious adverse effects among VAERS reports… For adverse events of special interest, it is reassuring that there were no unexpected signals other than myopericarditis and anaphylaxis, already known to be associated with mRNA vaccines."
Explore further Homologous Pfizer-BioNTech booster safe for adolescents
Large US study confirms most mRNA COVID-19 vaccine side effects are mild and temporary
A review of adverse events following vaccination against COVID-19 with mRNA vaccines in the U.S. confirms that most side effects were mild and decreased substantially after one day. The new study, published in The Lancet Infectious Diseases journal, suggests that for more than 298 million...
Large US study confirms most mRNA COVID-19 vaccine side effects are mild and temporary
by Lancet
March 7, 2022
A review of adverse events following vaccination against COVID-19 with mRNA vaccines in the U.S. confirms that most side effects were mild and decreased substantially after one day. The new study, published in The Lancet Infectious Diseases journal, suggests that for more than 298 million vaccine doses administered between December 2020 and June 2021, 92% (313,499/340,522) of reported adverse events were not serious, and less than 1% of v-safe participants reported seeking any medical care following vaccination.
In December 2020 two mRNA COVID-19 vaccines—Pfizer-BioNTech (BNT162b2) and Moderna (mRNA-1723) – were authorised for emergency use in the U.S.. Both vaccines involved two primary doses and have shown good safety profiles in clinical trials, with mild effects such as injection site pain, fatigue, and headache being reported as the most common adverse events.
As is the case for all vaccines in the U.S., anyone can report adverse events using the Vaccine Adverse Event Reporting System (VAERS), a long-standing reporting system run jointly by US Centers for Disease Control and Prevention (CDC) and the US Food and Drug Administration (FDA). With VAERS, US residents, their healthcare providers, or vaccine manufacturers can submit any event experienced following receipt of a vaccine. These reports are categorised as non-serious, serious, or death. The v-safe system, managed by CDC, was developed specifically for the COVID-19 vaccination programme, and consists of smartphone-based surveys sent daily for the first week after vaccination (and at longer time intervals in the months following) to monitor adverse reactions.
"Vaccines are the most effective tool to prevent serious COVID-19 disease outcomes and the benefits of immunisation in preventing serious illness and death strongly favour vaccination," says study author, Dr. Hannah Rosenblum, U.S. Centers for Disease Control and Prevention (CDC). "COVID-19 vaccine safety monitoring is the most robust in US history and the two complementary surveillance systems used in this study should bolster confidence that mRNA COVID-19 vaccines are safe."
This study looked at available VAERS and v-safe self-reported data between December 2020 and June 2021 following both doses of either the Pfizer-BioNTech or Moderna mRNA vaccines. During the study period, over 298 million doses of mRNA vaccines were administered (132 million Moderna and 167 million Pfizer).
VAERS received over 340,000 reports of adverse effects with more than 313,000 (92%) registered as non-serious, including headache (64,064/340,522 or 20%), fatigue (52,048/340,522 or 17%), fever (51,023/340,522 or 16%), chills (49,234/340,522 or 16%) and pain (47,745/340,522 or 15%). Of the more than 22,000 (6.6%) side effects registered as serious, the most common was shortness of breath (4,175/340,522 or 15%). Of 340,522 adverse events reported to VAERS during the study period, approximately 4500 (1.3%) were deaths, with more than 80% of these deaths among people ages 60 years or older. Because COVID-19 vaccines have been authorised under emergency use, healthcare providers are required to report all deaths following vaccination, regardless of the potential direct association. The study authors note that no unusual patterns were detected in cause death reports.
"The rapid pace at which COVID-19 vaccines were administered under emergency use, especially among older populations, was unprecedented. Due to their age, this group already has a higher baseline mortality rate than the general population and our results follow similar patterns of deaths rates for people in this age group following other adult vaccinations," says study author Dr. David Shay, also of the CDC.
Of the nearly 8 million v-safe participants, over half reported local (4.6 million) and systemic (3.6 million) reactions post-vaccination, occurring more frequently after dose two than dose one. Side effects were most frequently reported the day after vaccination and were nearly all mild, with the most common being fatigue (2,295,205/6,775,515 or 34% after dose one, 3,158,229/5,674,420 or 56% after dose two), headache (1,831,471/6,775,515 or 27% after dose one, 2,623,721/5,674,420 or 46% after dose two), and injection site pain (4,488,402/6,775,515 or 66% after dose one, 3,890,848/5,674,420 or 69% after dose two).
More v-safe reports of being unable to work, perform normal activities, or seeking medical care were reported after dose two (1,821,421/5,674,420 or 32%), than after dose one (808,963/6,775,515 or 12%). Less than 1% of participants (56,647 after dose one and 53,077 after dose two) reported seeking medical care after either vaccine dose.
Study author Dr. Tom Shimabukuro (US CDC) says: "VAERS and v-safe are important tools CDC can use when evaluating vaccine safety and to help identify any unexpected or unusual events. These data are reassuring that reactions to both mRNA vaccines are generally mild and subside after one or two days—confirming reports from clinical trials and post-authorization monitoring."
The authors acknowledge some limitations with this research. Firstly, the VAERS system relies on spontaneous reporting and is not representative of the entire population. This also means that while it can monitor for potential safety signals, it cannot define a causal relationship between vaccination and adverse events. This limitation lies with the surveillance system and not the study design. In addition, the need for smartphone access to participate in v-safe excludes populations without access to these devices. Finally, although trends in differences in adverse reactions have emerged among the Pfizer-BioNTech and Moderna mRNA vaccines, neither VAERS nor v-safe can definitively measure the safety differences between the two vaccines.
Writing in a linked comment, Elizabeth Phillips, Vanderbilt University Medical Center U.S., who was not involved in the study, said: "Reassuringly, the six-month VAERS data supports that, although approximately one in 1,000 individuals vaccinated may have an adverse effect, most of these are non-serious. No unusual patterns emerged in the cause of death or serious adverse effects among VAERS reports… For adverse events of special interest, it is reassuring that there were no unexpected signals other than myopericarditis and anaphylaxis, already known to be associated with mRNA vaccines."
Explore further Homologous Pfizer-BioNTech booster safe for adolescents
Safety of mRNA vaccines administered during the initial 6 months of the US COVID-19 vaccination programme: an observational study of reports to the Vaccine Adverse Event Reporting System and v-safe
Safety data from more than 298 million doses of mRNA COVID-19 vaccine administered in the first 6 months of the US vaccination programme show that most reported adverse events were mild and short in duration.
www.thelancet.com
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Genetic study gives extensive insights into severe COVID-19
The world's largest study of the genetics of critical COVID-19, involving more than 57,000 people, has revealed fresh details about some of the biological mechanisms behind the severe form of the disease.
Genetic study gives extensive insights into severe COVID-19
by University of Edinburgh
March 7, 2022
The world's largest study of the genetics of critical COVID-19, involving more than 57,000 people, has revealed fresh details about some of the biological mechanisms behind the severe form of the disease.
Some 16 new genetic variants associated with severe COVID-19, including some related to blood clotting, immune response and intensity of inflammation, have been identified.
These findings will act as a roadmap for future efforts, opening new fields of research focused on potential new therapies and diagnostics with pinpoint accuracy, experts say.
Researchers from the GenOMICC consortium—a global collaboration to study genetics in critical illness—led by University of Edinburgh in partnership with Genomics England, made these discoveries by sequencing the genomes of 7,491 patients from 224 intensive care units in the UK.
Their DNA was compared with 48,400 other people who had not had COVID-19, participants in Genomics England's 100,000 Genomes Project and that of a further 1,630 people who had experienced mild COVID.
Determining the whole genome sequence for all participants in the study allowed the team to create a precise map and identify genetic variation linked to severity of COVID-19. The team found key differences in 16 genes in the ICU patients when compared with the DNA of the other groups.
They also confirmed the involvement of seven other genetic variations already associated with severe COVID-19 discovered in earlier studies from the same team.
The findings included how a single gene variant that disrupts a key messenger molecule in immune system signaling—called interferon alpha-10—was enough to increase a patient's risk of severe disease.
This highlights the gene's key role in the immune system and suggests that treating patients with interferon—proteins released by immune cells to defend against viruses—may help manage disease in the early stages.
The study also found that variations in genes that control the levels of a central component of blood clotting—known as Factor 8—were associated with critical illness in COVID-19.
This may explain some of the clotting abnormalities that are seen in severe cases of COVID-19. Factor 8 is the gene underlying the most common type of hemophilia.
Professor Kenneth Baillie, the project's chief investigator and a Consultant in Critical Care Medicine at University of Edinburgh, said: "Our latest findings point to specific molecular targets in critical COVID-19. These results explain why some people develop life-threatening COVID-19, while others get no symptoms at all. But more importantly, this gives us a deep understanding of the process of disease and is a big step forward in finding more effective treatments.
"It is now true to say that we understand the mechanisms of COVID better than the other syndromes we treat in intensive care in normal times—sepsis, flu, and other forms of critical illness. COVID-19 is showing us the way to tackle those problems in the future."
Professor Sir Mark Caulfield from Queen Mary University of London, formerly Chief Scientist at Genomics England and co-author on this study, said: "As COVID-19 evolves, we need to focus on reducing the number of people getting seriously ill and being hospitalized. Through our whole genome sequencing research, we've discovered novel gene variants that predispose people to severe illness—which now offer a route to new tests and treatments, to help protect the public and the NHS from this virus."
Dr. Rich Scott, Chief Medical Officer at Genomics England, said: "Strategically, we're at a point where genomic science is becoming an integral part of the national infrastructure in routine healthcare. This study illustrates the value of whole genome sequencing to detect rare and common variants that influence critical illness requiring intensive care. It represents a major leap forward in our understanding of how our genetic makeup influences severe illness with COVID-19."
"All those involved in the study went to great efforts to engage with all communities within the UK—including groups that have historically been under-represented in medical studies. The inclusive element of our work has generated meaningful results for everyone in the country."
Lord Kamall, Minister for innovation at the Department of Health and Social Care (DHSC), said: "Clinical research has been vital in our fight against COVID-19 and the UK's innovation is enabling us to transform our health service and ensure the NHS is able to deliver world-class care.
"This research is an important step forward in better understanding how COVID-19 impacts certain people, allowing us to take the necessary action to protect the most vulnerable and save lives."
The findings have been published in Nature.
GenOMICC (Genetics of Susceptibility and Mortality in Critical Care) started in 2015 as an open, global consortium of intensive care clinicians dedicated to understanding genetic factors influencing outcomes in intensive care from diseases such as SARS, flu and sepsis.
The ground-breaking 100,000 Genomes Project was established in 2014 to sequence 100,000 genomes from people with a rare disease or cancer. The Project was completed in 2018 and paved the way for the creation of a new genomic medicine service for NHS England, transforming patient care by bringing advanced diagnosis and personalized treatments.
Explore further Genes could be key to new COVID-19 treatments, study finds
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'Immune distraction' from previous colds leads to worse COVID infections
At the beginning of the COVID pandemic, we were hopeful that pre-existing immunity to the common cold could protect you from COVID, but new evidence suggests that sometimes the opposite can happen. A new University of Rochester Medical Center study shows that prior infection and immunity to one...
'Immune distraction' from previous colds leads to worse COVID infections
by University of Rochester
March 7, 2022
At the beginning of the COVID pandemic, we were hopeful that pre-existing immunity to the common cold could protect you from COVID, but new evidence suggests that sometimes the opposite can happen. A new University of Rochester Medical Center study shows that prior infection and immunity to one of the common cold coronaviruses may have put people at risk of more severe COVID illness and death.
The study, published in the Journal of Infectious Diseases, examined immunity to various coronaviruses, including the COVID-causing SARS-CoV-2 virus, in blood samples taken from 155 COVID patients in the early months of the pandemic. Of those patients, 112 were hospitalized and provided sequential samples over the course of their hospitalization.
These hospitalized patients experienced a large, rapid increase in antibodies that targeted SARS-CoV-2 and several other coronaviruses. While big boosts in antibodies—protective proteins generated by the immune system—is usually a good thing, in this case, it wasn't.
The study showed that these antibodies were targeting parts of the spike protein (which sits on the surface of coronaviruses and helps them infect cells) that were similar to common cold coronaviruses the immune system remembered from previous infections. Unfortunately, targeting those areas meant the antibodies could not neutralize the new SARS-CoV-2 virus. When levels of these antibodies rose faster than levels of SARS-CoV-2 neutralizing antibodies, patients had worse disease and a higher chance of death.
"In people who were sicker—those who were in the ICU or died in the hospital, the immune system was responding robustly in a way that was less protective," said lead study author Martin Zand, M.D., Ph.D., who is the senior associate dean of Clinical Research at URMC. "It took those patients longer for the immune system to make protective antibodies… unfortunately, too late for some."
This study adds to a growing pool of evidence that a phenomenon called immune imprinting is at play in COVID immune responses. Zand, who is also a co-director of the University of Rochester Clinical and Translational Science Institute (UR CTSI), likens this phenomenon to 'immune distraction': immunity to one threat (seasonal coronaviruses) hijacks the immune response to a new, but similar threat (SARS-CoV-2). Immune imprinting has been linked to poor immune responses to other viruses, like flu, and can have implications for vaccine strategies.
By some predictions, COVID is likely to be with us for a long time—with new, milder strains emerging and circulating on an annual or seasonal basis. If those predictions hold true, the study suggests that we will need to regularly develop new vaccines targeting the new strains of SARS-CoV-2. While none have come to market yet, pharmaceutical companies like Pfizer and Moderna have been developing and testing new versions of their COVID vaccines as new variants of concern have emerged.
"We should expect that development of new vaccines is a good thing," said Zand. "It doesn't mean the original science was wrong. It means nature has changed. If we want an immune system that pays attention to the right stuff, we need to teach it new tricks with different vaccines."
The study also analyzed 188 blood samples collected in the pre-COVID era (prior to December of 2019) as controls. Some of the blood samples analyzed for the study were provided by the UR CTSI's COVID-19 Biobank, a repository of blood samples from hundreds of patients with and without COVID infections that was developed by the UR CTSI and URMC Shared Resource Labs.
Explore further Common cold coronaviruses hinder antibody immune response to SARS-CoV-2 infection
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The U.S. Government Invested Over a Billion Dollars in Promoting Pro-COVID Vaccine Narratives .49 min
The U.S. Government Invested Over a Billion Dollars in Promoting Pro-COVID Vaccine Narratives
Red Voice Media Published March 7, 2022 234 Views
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FAKE HYDROXYCHLOROQUINE STUDY EXPOSES CORRUPTION AT THE HIGHEST LEVELS - DR. RICHARD URSO 4:07 min
FAKE HYDROXYCHLOROQUINE STUDY EXPOSES CORRUPTION AT THE HIGHEST LEVELS - DR. RICHARD URSO
The U.S. Government Invested Over a Billion Dollars in Promoting Pro-COVID Vaccine Narratives
Red Voice Media Published March 7, 2022 234 Views
^^^^^
FAKE HYDROXYCHLOROQUINE STUDY EXPOSES CORRUPTION AT THE HIGHEST LEVELS - DR. RICHARD URSO 4:07 min
FAKE HYDROXYCHLOROQUINE STUDY EXPOSES CORRUPTION AT THE HIGHEST LEVELS - DR. RICHARD URSO
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Lancet published the SurgiSphere paper.I am posting this because it's from the Lancet, as mainstream as you can get for 'medical news'. This is a news thread, so I'm posting what this reputable publication is telling the population that looks to them for medical news.
(fair use applies)Large US study confirms most mRNA COVID-19 vaccine side effects are mild and temporary
A review of adverse events following vaccination against COVID-19 with mRNA vaccines in the U.S. confirms that most side effects were mild and decreased substantially after one day. The new study, published in The Lancet Infectious Diseases journal, suggests that for more than 298 million...
Large US study confirms most mRNA COVID-19 vaccine side effects are mild and temporary
by Lancet
March 7, 2022
A review of adverse events following vaccination against COVID-19 with mRNA vaccines in the U.S. confirms that most side effects were mild and decreased substantially after one day. The new study, published in The Lancet Infectious Diseases journal, suggests that for more than 298 million vaccine doses administered between December 2020 and June 2021, 92% (313,499/340,522) of reported adverse events were not serious, and less than 1% of v-safe participants reported seeking any medical care following vaccination.
In December 2020 two mRNA COVID-19 vaccines—Pfizer-BioNTech (BNT162b2) and Moderna (mRNA-1723) – were authorised for emergency use in the U.S.. Both vaccines involved two primary doses and have shown good safety profiles in clinical trials, with mild effects such as injection site pain, fatigue, and headache being reported as the most common adverse events.
As is the case for all vaccines in the U.S., anyone can report adverse events using the Vaccine Adverse Event Reporting System (VAERS), a long-standing reporting system run jointly by US Centers for Disease Control and Prevention (CDC) and the US Food and Drug Administration (FDA). With VAERS, US residents, their healthcare providers, or vaccine manufacturers can submit any event experienced following receipt of a vaccine. These reports are categorised as non-serious, serious, or death. The v-safe system, managed by CDC, was developed specifically for the COVID-19 vaccination programme, and consists of smartphone-based surveys sent daily for the first week after vaccination (and at longer time intervals in the months following) to monitor adverse reactions.
"Vaccines are the most effective tool to prevent serious COVID-19 disease outcomes and the benefits of immunisation in preventing serious illness and death strongly favour vaccination," says study author, Dr. Hannah Rosenblum, U.S. Centers for Disease Control and Prevention (CDC). "COVID-19 vaccine safety monitoring is the most robust in US history and the two complementary surveillance systems used in this study should bolster confidence that mRNA COVID-19 vaccines are safe."
This study looked at available VAERS and v-safe self-reported data between December 2020 and June 2021 following both doses of either the Pfizer-BioNTech or Moderna mRNA vaccines. During the study period, over 298 million doses of mRNA vaccines were administered (132 million Moderna and 167 million Pfizer).
VAERS received over 340,000 reports of adverse effects with more than 313,000 (92%) registered as non-serious, including headache (64,064/340,522 or 20%), fatigue (52,048/340,522 or 17%), fever (51,023/340,522 or 16%), chills (49,234/340,522 or 16%) and pain (47,745/340,522 or 15%). Of the more than 22,000 (6.6%) side effects registered as serious, the most common was shortness of breath (4,175/340,522 or 15%). Of 340,522 adverse events reported to VAERS during the study period, approximately 4500 (1.3%) were deaths, with more than 80% of these deaths among people ages 60 years or older. Because COVID-19 vaccines have been authorised under emergency use, healthcare providers are required to report all deaths following vaccination, regardless of the potential direct association. The study authors note that no unusual patterns were detected in cause death reports.
"The rapid pace at which COVID-19 vaccines were administered under emergency use, especially among older populations, was unprecedented. Due to their age, this group already has a higher baseline mortality rate than the general population and our results follow similar patterns of deaths rates for people in this age group following other adult vaccinations," says study author Dr. David Shay, also of the CDC.
Of the nearly 8 million v-safe participants, over half reported local (4.6 million) and systemic (3.6 million) reactions post-vaccination, occurring more frequently after dose two than dose one. Side effects were most frequently reported the day after vaccination and were nearly all mild, with the most common being fatigue (2,295,205/6,775,515 or 34% after dose one, 3,158,229/5,674,420 or 56% after dose two), headache (1,831,471/6,775,515 or 27% after dose one, 2,623,721/5,674,420 or 46% after dose two), and injection site pain (4,488,402/6,775,515 or 66% after dose one, 3,890,848/5,674,420 or 69% after dose two).
More v-safe reports of being unable to work, perform normal activities, or seeking medical care were reported after dose two (1,821,421/5,674,420 or 32%), than after dose one (808,963/6,775,515 or 12%). Less than 1% of participants (56,647 after dose one and 53,077 after dose two) reported seeking medical care after either vaccine dose.
Study author Dr. Tom Shimabukuro (US CDC) says: "VAERS and v-safe are important tools CDC can use when evaluating vaccine safety and to help identify any unexpected or unusual events. These data are reassuring that reactions to both mRNA vaccines are generally mild and subside after one or two days—confirming reports from clinical trials and post-authorization monitoring."
The authors acknowledge some limitations with this research. Firstly, the VAERS system relies on spontaneous reporting and is not representative of the entire population. This also means that while it can monitor for potential safety signals, it cannot define a causal relationship between vaccination and adverse events. This limitation lies with the surveillance system and not the study design. In addition, the need for smartphone access to participate in v-safe excludes populations without access to these devices. Finally, although trends in differences in adverse reactions have emerged among the Pfizer-BioNTech and Moderna mRNA vaccines, neither VAERS nor v-safe can definitively measure the safety differences between the two vaccines.
Writing in a linked comment, Elizabeth Phillips, Vanderbilt University Medical Center U.S., who was not involved in the study, said: "Reassuringly, the six-month VAERS data supports that, although approximately one in 1,000 individuals vaccinated may have an adverse effect, most of these are non-serious. No unusual patterns emerged in the cause of death or serious adverse effects among VAERS reports… For adverse events of special interest, it is reassuring that there were no unexpected signals other than myopericarditis and anaphylaxis, already known to be associated with mRNA vaccines."
Explore further Homologous Pfizer-BioNTech booster safe for adolescents
Safety of mRNA vaccines administered during the initial 6 months of the US COVID-19 vaccination programme: an observational study of reports to the Vaccine Adverse Event Reporting System and v-safe
Safety data from more than 298 million doses of mRNA COVID-19 vaccine administered in the first 6 months of the US vaccination programme show that most reported adverse events were mild and short in duration.www.thelancet.com
Heliobas Disciple
TB Fanatic
Lancet is going the direction of the NYT. For decades the most trustworthy and neutral source of news. If it was in the Times, you could take it to the bank, blah blah blah. Now it's just a political rag. Seems the Lancet is following suit...
Heliobas Disciple
TB Fanatic
The next 5 articles are from Profit of Doom who has trouble posting articles from his phone. the first one is an older article from robert malone, i will post it first. It may have been posted when it first came out, I didn't search up the thread to see.
rwmalonemd.substack.com
(fair use applies)
A Health Public Policy Nightmare
Vaccine spike antigen and mRNA persist for two months in lymph node germinal centers...
Robert W Malone MD, MS
Feb 8
Immune imprinting, breadth of variant recognition and germinal center response in human SARS-CoV-2 infection and vaccination Cell. Published:January 24, 2022DOI:Redirecting
Highlights (per the journal)
One very real hypothesis is that the substitution of pseudouridine for uridine to avoid the immune response is working so well that the mRNA is completely evading the normal clearance/degradation pathways. Hence, mRNA that is not being incorporated into cells at the injection site, is migrating to the lymph nodes (and throughout the body as the non-clinical Pfizer data suggest?) and continuing to express protein there. In this case, the cytotoxic protein antigen is spike. Spike protein can be detected for at least 2+ weeks after administration of dose. It did not appear that spike protein was tested for later than that, although the study is poorly worded in this regard. Nevertheless, abundant spike protein was detected after vaccination that continues for an indefinite time.
The spike protein, let’s review what it is and how it is being used (from the Daily Skeptic):
That this has not been published or investigated more demonstrates the gross regulatory dereliction of duty by Pfizer, Biointech, Moderna, NIAID VRC and that whole crew. Using these vaccines, which include pseudouridine without fully understanding the implications and without the FDA requiring a complete pre-clinical toxicology regulatory package, including long-term follow-up, as is done with any other unique chemical or adjuvant additive is shocking. Then there is the novel use of the unique nano particles being used in these vaccines, which also were only marginally assessed, as shown by the Japanese Pfizer data.
Protein expression is not being turned off, because the immune response against the mRNA/pseudouridine complex is either not happening or is ineffective. It may also be that the mRNA/pseudouridine complex has a longer half-life than normal mRNA. The In either case, this is regulatory nightmare.
I do not know how to write this more strongly. This technology is immature. The WHO has approved six, more traditional vaccines, all of which the US government could license. These genetic vaccines are not the only option.
To note: The use of pseudouridine in these mRNA vaccines is not the only option. It has often been hypothesized that the reason Dr. Kariko added pseudouridine to the mRNA vaccine was to make an improvement to the original mRNA patents that I was an inventor on. An improvement to an existing patent allows commercialization of that patent. It is an old trick. Remember, that Curevac does not use pseudouridine in its formulation and it is not required or necessary for a significant immune response. In the next generation of mRNA vaccine experiments (hopefully done in an animal model), it is clear that the issues of adding pseudouridine need to be addressed prior to any more of these vaccines going into humans.
I know the following from the paper is long, but it is very important.
Prolonged detection of vaccine mRNA in LN GCs, and spike antigen in LN GCs and blood following SARS-CoV-2 mRNA vaccination
This Substack article has only skimmed the surface of the implications of this paper in terms of both the science and the malfeasance on the part of our government and pharmaceutical corporations. There is more to come on this issue.
To get to the full paper to download, click here.
Why Weren’t These Vaccines Put Through the Proper Safety Trials For Gene Technology, Asks a Former Pharmaceutical Research Scientist The Daily Skeptic 7 February 2022 by Dr. John D. Flack
This article by the daily skeptic does a great job at documenting that appropriate studies have not been done and even attempts to answer the question why:
A Health Public Policy Nightmare
Vaccine spike antigen and mRNA persist for two months in lymph node germinal centers...
rwmalonemd.substack.com
A Health Public Policy Nightmare
Vaccine spike antigen and mRNA persist for two months in lymph node germinal centers...
Robert W Malone MD, MS
Feb 8
Immune imprinting, breadth of variant recognition and germinal center response in human SARS-CoV-2 infection and vaccination Cell. Published:January 24, 2022DOI:Redirecting
Highlights (per the journal)
- Vaccination confers broader IgG binding of variant RBDs than SARS-CoV-2 infection
- Imprinting from initial antigen exposures alters IgG responses to viral variants
- Histology of mRNA vaccinee lymph nodes shows abundant germinal centers
- Vaccine spike antigen and mRNA persist for weeks in lymph node germinal centers
One very real hypothesis is that the substitution of pseudouridine for uridine to avoid the immune response is working so well that the mRNA is completely evading the normal clearance/degradation pathways. Hence, mRNA that is not being incorporated into cells at the injection site, is migrating to the lymph nodes (and throughout the body as the non-clinical Pfizer data suggest?) and continuing to express protein there. In this case, the cytotoxic protein antigen is spike. Spike protein can be detected for at least 2+ weeks after administration of dose. It did not appear that spike protein was tested for later than that, although the study is poorly worded in this regard. Nevertheless, abundant spike protein was detected after vaccination that continues for an indefinite time.
The spike protein, let’s review what it is and how it is being used (from the Daily Skeptic):
These new gene-based ‘vaccines’ are working in a completely novel way – nothing remotely resembling that of traditional vaccines. Given that pharmaceutical companies work competitively it was also somewhat of a surprise they took the same approach of targeting what has been termed the ‘spike protein’ of the SARS-CoV-2 virus.
This (spike) protein is nasty – sometimes being referred to as a ‘pathogenic protein’ – and is recognised as causing many of the awful pathologies associated with the disease of COVID-19. Logically you would inactivate or at least attenuate this nasty spike protein and develop a vaccine around the attenuated virus. But that’s not what was done. These ‘vaccines’ do not contain any of the offending virus at all but rather the gene sequence that causes the nasty spike protein to be made in the body. We have little idea how much of this nasty protein is produced or for how long it lasts after an injection of the gene sequence. Furthermore, stimulating the body’s own complex biological systems to produce the spike protein will mean that the amount of protein produced will vary from person to person. The idea is that the spike protein produced by the gene encoding it elicits a response by our immune system to produce antibodies directed against the spike. When the wild virus comes along and infects us the antibodies recognise the spike protein and attack it thus preventing its nasty effects. And it does, though as we have since learnt this approach isn’t very good at preventing infection or stopping its transmission. Are we perhaps clutching at straws too in claiming that these ‘vaccines’ are preventing serious disease and death? Have we not learnt anything over the past two years in treating Covid symptoms with conventional therapeutic drugs?
Knowing what we know about the spike protein in these vaccines, the study quantitatively measured spike protein levels in plasma after vaccination. This should have been characterized long ago, including prior to beginning human clinical trials.That this has not been published or investigated more demonstrates the gross regulatory dereliction of duty by Pfizer, Biointech, Moderna, NIAID VRC and that whole crew. Using these vaccines, which include pseudouridine without fully understanding the implications and without the FDA requiring a complete pre-clinical toxicology regulatory package, including long-term follow-up, as is done with any other unique chemical or adjuvant additive is shocking. Then there is the novel use of the unique nano particles being used in these vaccines, which also were only marginally assessed, as shown by the Japanese Pfizer data.
Protein expression is not being turned off, because the immune response against the mRNA/pseudouridine complex is either not happening or is ineffective. It may also be that the mRNA/pseudouridine complex has a longer half-life than normal mRNA. The In either case, this is regulatory nightmare.
I do not know how to write this more strongly. This technology is immature. The WHO has approved six, more traditional vaccines, all of which the US government could license. These genetic vaccines are not the only option.
To note: The use of pseudouridine in these mRNA vaccines is not the only option. It has often been hypothesized that the reason Dr. Kariko added pseudouridine to the mRNA vaccine was to make an improvement to the original mRNA patents that I was an inventor on. An improvement to an existing patent allows commercialization of that patent. It is an old trick. Remember, that Curevac does not use pseudouridine in its formulation and it is not required or necessary for a significant immune response. In the next generation of mRNA vaccine experiments (hopefully done in an animal model), it is clear that the issues of adding pseudouridine need to be addressed prior to any more of these vaccines going into humans.
I know the following from the paper is long, but it is very important.
Prolonged detection of vaccine mRNA in LN GCs, and spike antigen in LN GCs and blood following SARS-CoV-2 mRNA vaccination
The biodistribution, quantity and persistence of vaccine mRNA and spike antigen after vaccination (with the Pfizer vaccine), and viral antigens after SARS-CoV-2 infection, are incompletely understood but are likely to be major determinants of immune responses. We performed in situ hybridization with control and SARS-CoV-2 vaccine mRNA-specific RNAScope probes in the core needle biopsies of the ipsilateral axillary LNs that were collected 7-60 days after 2nd dose of mRNA-1273 or BNT162b2 vaccination, and detected vaccine mRNA collected in the GCs of LNs on day 7, 16, and 37 post vaccination, with lower but still appreciable specific signal at day 60 (Figures 7A -7E). Only rare foci of vaccine mRNA were seen outside of GCs. Axillary LN core needle biopsie of non-vaccinees (n = 3) and COVID-19 patient specimens were negative for vaccine probe hybridization.
Immunohistochemical staining for spike antigen in mRNA vaccinated patient LNs varied between individuals, but showed abundant spike protein in GCs 16 days post-2nd dose, with spike antigen still present as late as 60 days post-2nd dose. Spike antigen localized in a reticular pattern around the GC cells, similar to staining for follicular dendritic cell processes (Figure 7B). COVID-19 patient LNs showed lower quantities of spike antigen, but a rare GC had positive staining (Figure 7F). Immunohistochemical staining for N antigen in peribronchial LN secondary and primary follicles of COVID-19 patients (Figures 7F - 7I) was positive in 5 of the 7 patients, with a mean percentage of nucleocapsid-positive follicles of more than 25%.
Discussion One of the positive developments amid the global calamity of the SARS-CoV-2 pandemic has been the rapid design, production and deployment of a variety of vaccines, including remarkably effective mRNA vaccines encoding the viral spike (Baden et al., 2021; Polack et al., 2020). We find that BNT162b2 vaccination produces IgG responses to spike and RBD at concentrations as high as those of severely ill COVID-19 patients and follows a similar time course. Unlike infection, which stimulates robust but short-lived IgM and IgA responses, vaccination shows a pronounced bias for IgG production even at early time point
This Substack article has only skimmed the surface of the implications of this paper in terms of both the science and the malfeasance on the part of our government and pharmaceutical corporations. There is more to come on this issue.
To get to the full paper to download, click here.
Why Weren’t These Vaccines Put Through the Proper Safety Trials For Gene Technology, Asks a Former Pharmaceutical Research Scientist The Daily Skeptic 7 February 2022 by Dr. John D. Flack
This article by the daily skeptic does a great job at documenting that appropriate studies have not been done and even attempts to answer the question why:
Are we perhaps clutching at straws too in claiming that these ‘vaccines’ are preventing serious disease and death? Have we not learnt anything over the past two years in treating Covid symptoms with conventional therapeutic drugs?
Perhaps this has driven Big Pharma to pursue a new more profitable model based on protecting the healthy rather than treating the sick? Enter the era of the gene-based ‘vaccines’. The new technologies have had a long and difficult gestation period with several stillbirths. But perhaps their time had come with the ‘unprecedented’ virus from the East. A declared worldwide health emergency demanded a technological response, and it was there in waiting. But have we been blinded and duped by technology and lost sight of the end game of providing safe and effective medicines? Was it a judicious use of the PCR, rapid antigen test technology and information APP technology to drive the test and trace fiasco?
Was the gene technology ready to be used in a mass world-wide vaccination programme without a thorough examination of the potential problems of short- and long-term safety of this previously untested technology?
In my view, technocracy has trumped the sound principles, established over decades and centuries, of basic medical practice, immunology, virology, pharmaceutical sciences and public health generally. In the process, political democracy, personal freedoms, free speech and choice have been dangerously sidelined and even censored.
.
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Heliobas Disciple
TB Fanatic
Article 2 from Profit of Doom. this one is from last May, also didn't check to see if already been posted up thread.
www.clarkcountytoday.com
(fair use applies)
Opinion: We should be questioning the global suppression of early treatment options for COVID-19
Clark County Today Administrator Heidi Wetzler shares what she believes is a medical tragedy that COVID-19 patients are not being treated immediately
Posted by Heidi Wetzler
Date: Thursday, May 27, 2021
If you walked into your doctor’s office with a case of shingles, what do you think would happen? Would you be sent home and instructed to return when the pain was unbearable – or would you be treated on the spot? While there is no cure for shingles, prompt treatment with prescription antiviral drugs can speed healing and reduce the risk of complications.
What about viral pneumonia, viral hepatitis, or HIV/Aids? Same question. Would you be treated? The answer of course, is yes. These all have treatment protocols, to speed recovery and increase comfort, even though viruses don’t necessarily have “cures.” Because viruses don’t respond to antibiotics, alternative treatments are important. And they all work best when started early. So why do we have a fatal viral infection ravaging the world, with barely a mention of ambulatory treatment?
Millions of people have tested positive for COVID-19, and are promptly sent home to quarantine and self-monitor their symptoms. No health care professional checks in on them. They are told to stay home and only come back if they are having trouble breathing. While I would imagine it is common knowledge in the medical community that early treatment for any ailment greatly improves the chance of a favorable outcome, why is there a virtual blackout of information surrounding the global conversation of early treatment protocol in order to AVOID hospitalization and death? Controlling the healthy with masks and social distancing and now vaccines, and then Herculean efforts involving the critically ill, have taken up all of the air, while the person in their first two weeks of the infection suffering at home is all but ignored by the medical community.
Dr. Peter McCullough, vice chief of Internal Medicine at Baylor University Medical Center in Dallas, Texas, and the most prolifically published academic physician in his field of heart and kidneys in history, has testified several times lately that there is a shocking suppression of early treatment for COVID-19 in medical literature. A review of several of his communications resulted in this summary of his findings. He calls this effort to suppress any hope of treatment, extraordinary. All of the patients he sees are considered high risk, and with the sequenced multi-drug approach he uses, he has only lost two. When he extrapolates the data he has personally acquired through treating his own very ill patients, and calculates what that would mean for the death rate worldwide if a similar treatment protocol was adopted globally, an astonishing 85 percent of COVID-19 deaths could have been prevented. The key is that treatment must begin early in order to avoid hospitalization. And that is the opposite of what has happened and is continuing to happen.
The treatment regimen includes 4-6 drugs taken in a specific time frame, starting with monoclonal antibodies, then antivirals, then anti-inflammatories, and then anticoagulants. It is recommended that anyone over 50 with at least one comorbidity begin this course of treatment immediately. Reduction of viral replication at the forefront of infection is key. There has been unconventional concern worldwide regarding the safety of certain therapeutics for this virus. In fact, in Australia doctors were threatened with a 6-month prison sentence if they dared to prescribe the antiviral, Hydroxychloroquine. This move is unprecedented. The use of Hydroxychloroquine for COVID-19 is off-label they said. But off-label use of older medicines for new uses occurs every day. In fact, 20 percent of all prescriptions in the U.S. are written for off-label uses when a doctor thinks a medicine will benefit a patient. Apparently, the list of what not to use is long and broad within the treatment recommendations. We are 16 months into this thing and as-of-yet, there are zero trials of multidrug therapies. There is no national or global panel of doctors in charge of early treatment protocol. Why? Maybe it’s because a vaccine is only allowed to be produced if there are no effective treatments.
The conversation around building up one’s own immune system is also nearly nonexistent in medical and mainstream circles. A study conducted from March-June 2020 including 191,000 patients in the US found that Vitamin D deficiency increased the risk of acquiring COVID-19 by 54.5 percent. Additionally, 80 percent of people with COVID-19 didn’t have adequate levels of the vitamin in their blood. This is a wildly important piece of information that doctors should be shouting from the rooftops. Zinc is also critical as it helps block the virus from multiplying. An Adult Treatment Guide put out by Yale University cites “a lack of clinical data to support” the effectiveness of various vitamins and medicines. It is high time for the medical community to be implementing trials of all kinds and gathering such data. But the sole focus today seems to be on a one-size-fits-all vaccination campaign, instead of on strengthening one’s immune system and finding effective treatments. All of the eggs in the proverbial COVID-19 basket seem to be filled with only one treatment – the vaccine.
Dr. McCullough testifies that there is no scientific rationale to vaccinate anyone under the age of 50. The individual risk outweighs the individual benefit. Also, there were several groups that were intentionally excluded from the Moderna, Pfizer, and Johnson & Johnson vaccine trials in 2020; COVID-19 recovered, suspected COVID-19 recovered, those with COVID-19 antibodies, pregnant women, and women of childbearing potential that couldn’t assure the use of contraceptives. Pregnant women as a rule of best medical practice are always discouraged from coming in contact with anything pathogenic. The COVID-19 vaccine produces a pathogenic protein. Why then, are pregnant women being given the shot? The existing scientific data simply does not ensure that it is safe for this group. My family is COVID-19 recovered. Why are we being encouraged to participate when our situation was not included in the clinical trial? Whether we want to believe it or not, COVID-19 recovered individuals are unknowingly signing up for a trial now if they receive the vaccine.
Historically, those who contract and recover from a virus, have robust, complete and durable immunity. COVID-19 recovered, have actually been found to possess a terrific track record of freedom from reinfection. Moreover, SARS-coV-1, which emerged from China in 2002 is 79 percent similar to SARS-coV-2 (COVID-19), and most of those who contracted SARS-coV-1 still had immunity 17 years later. It is a false narrative at this point to suggest that there is significant concern that you can get it twice. While it is possible, it is now known that the chances are extremely low. On top of that those with natural immunity cannot acquire or spread it, as is a concern with those whose only immunity is from the vaccine.
What we are witnessing now is tremendous coercion for everyone to receive this vaccine, no matter the individual risk/benefit analysis. This strategy is in direct opposition to The Nuremberg Code which doctors profess to uphold. The first tenet of this code begins as follows:
The Association of American Physicians and Surgeons have put out a guide to Home-Based COVID treatment. A copy can be found here. There are 35 treatment centers in Texas for early treatment of COVID and if you need help finding one near you, there is a link to a list within this guide. As a society, we need to be questioning the radical suppression of early treatment options for a potentially fatal virus. It simply makes no logical sense.
.
Opinion: We should be questioning the global suppression of early treatment options for COVID-19
Clark County Today Administrator Heidi Wetzler shares what she believes is a medical tragedy that COVID-19 patients are not being treated immediately.
www.clarkcountytoday.com
Opinion: We should be questioning the global suppression of early treatment options for COVID-19
Clark County Today Administrator Heidi Wetzler shares what she believes is a medical tragedy that COVID-19 patients are not being treated immediately
Posted by Heidi Wetzler
Date: Thursday, May 27, 2021
If you walked into your doctor’s office with a case of shingles, what do you think would happen? Would you be sent home and instructed to return when the pain was unbearable – or would you be treated on the spot? While there is no cure for shingles, prompt treatment with prescription antiviral drugs can speed healing and reduce the risk of complications.
What about viral pneumonia, viral hepatitis, or HIV/Aids? Same question. Would you be treated? The answer of course, is yes. These all have treatment protocols, to speed recovery and increase comfort, even though viruses don’t necessarily have “cures.” Because viruses don’t respond to antibiotics, alternative treatments are important. And they all work best when started early. So why do we have a fatal viral infection ravaging the world, with barely a mention of ambulatory treatment?
Millions of people have tested positive for COVID-19, and are promptly sent home to quarantine and self-monitor their symptoms. No health care professional checks in on them. They are told to stay home and only come back if they are having trouble breathing. While I would imagine it is common knowledge in the medical community that early treatment for any ailment greatly improves the chance of a favorable outcome, why is there a virtual blackout of information surrounding the global conversation of early treatment protocol in order to AVOID hospitalization and death? Controlling the healthy with masks and social distancing and now vaccines, and then Herculean efforts involving the critically ill, have taken up all of the air, while the person in their first two weeks of the infection suffering at home is all but ignored by the medical community.
Dr. Peter McCullough, vice chief of Internal Medicine at Baylor University Medical Center in Dallas, Texas, and the most prolifically published academic physician in his field of heart and kidneys in history, has testified several times lately that there is a shocking suppression of early treatment for COVID-19 in medical literature. A review of several of his communications resulted in this summary of his findings. He calls this effort to suppress any hope of treatment, extraordinary. All of the patients he sees are considered high risk, and with the sequenced multi-drug approach he uses, he has only lost two. When he extrapolates the data he has personally acquired through treating his own very ill patients, and calculates what that would mean for the death rate worldwide if a similar treatment protocol was adopted globally, an astonishing 85 percent of COVID-19 deaths could have been prevented. The key is that treatment must begin early in order to avoid hospitalization. And that is the opposite of what has happened and is continuing to happen.
The treatment regimen includes 4-6 drugs taken in a specific time frame, starting with monoclonal antibodies, then antivirals, then anti-inflammatories, and then anticoagulants. It is recommended that anyone over 50 with at least one comorbidity begin this course of treatment immediately. Reduction of viral replication at the forefront of infection is key. There has been unconventional concern worldwide regarding the safety of certain therapeutics for this virus. In fact, in Australia doctors were threatened with a 6-month prison sentence if they dared to prescribe the antiviral, Hydroxychloroquine. This move is unprecedented. The use of Hydroxychloroquine for COVID-19 is off-label they said. But off-label use of older medicines for new uses occurs every day. In fact, 20 percent of all prescriptions in the U.S. are written for off-label uses when a doctor thinks a medicine will benefit a patient. Apparently, the list of what not to use is long and broad within the treatment recommendations. We are 16 months into this thing and as-of-yet, there are zero trials of multidrug therapies. There is no national or global panel of doctors in charge of early treatment protocol. Why? Maybe it’s because a vaccine is only allowed to be produced if there are no effective treatments.
The conversation around building up one’s own immune system is also nearly nonexistent in medical and mainstream circles. A study conducted from March-June 2020 including 191,000 patients in the US found that Vitamin D deficiency increased the risk of acquiring COVID-19 by 54.5 percent. Additionally, 80 percent of people with COVID-19 didn’t have adequate levels of the vitamin in their blood. This is a wildly important piece of information that doctors should be shouting from the rooftops. Zinc is also critical as it helps block the virus from multiplying. An Adult Treatment Guide put out by Yale University cites “a lack of clinical data to support” the effectiveness of various vitamins and medicines. It is high time for the medical community to be implementing trials of all kinds and gathering such data. But the sole focus today seems to be on a one-size-fits-all vaccination campaign, instead of on strengthening one’s immune system and finding effective treatments. All of the eggs in the proverbial COVID-19 basket seem to be filled with only one treatment – the vaccine.
Dr. McCullough testifies that there is no scientific rationale to vaccinate anyone under the age of 50. The individual risk outweighs the individual benefit. Also, there were several groups that were intentionally excluded from the Moderna, Pfizer, and Johnson & Johnson vaccine trials in 2020; COVID-19 recovered, suspected COVID-19 recovered, those with COVID-19 antibodies, pregnant women, and women of childbearing potential that couldn’t assure the use of contraceptives. Pregnant women as a rule of best medical practice are always discouraged from coming in contact with anything pathogenic. The COVID-19 vaccine produces a pathogenic protein. Why then, are pregnant women being given the shot? The existing scientific data simply does not ensure that it is safe for this group. My family is COVID-19 recovered. Why are we being encouraged to participate when our situation was not included in the clinical trial? Whether we want to believe it or not, COVID-19 recovered individuals are unknowingly signing up for a trial now if they receive the vaccine.
Historically, those who contract and recover from a virus, have robust, complete and durable immunity. COVID-19 recovered, have actually been found to possess a terrific track record of freedom from reinfection. Moreover, SARS-coV-1, which emerged from China in 2002 is 79 percent similar to SARS-coV-2 (COVID-19), and most of those who contracted SARS-coV-1 still had immunity 17 years later. It is a false narrative at this point to suggest that there is significant concern that you can get it twice. While it is possible, it is now known that the chances are extremely low. On top of that those with natural immunity cannot acquire or spread it, as is a concern with those whose only immunity is from the vaccine.
What we are witnessing now is tremendous coercion for everyone to receive this vaccine, no matter the individual risk/benefit analysis. This strategy is in direct opposition to The Nuremberg Code which doctors profess to uphold. The first tenet of this code begins as follows:
Simply put, each person gets to decide what happens to their body. We are witnessing all manner of coercion regarding the distribution of this vaccine. Free donuts, lottery-style winnings, reduced prison sentences, and pressure from Hollywood stars. The weird and wild list goes on and on. Schools are offering vaccine clinics around the world, some without requiring the consent of parents. There simply is no significant evidence that children are at risk of spreading or becoming sick or dying from this virus. To me, these actions are nothing short of criminal.
The Association of American Physicians and Surgeons have put out a guide to Home-Based COVID treatment. A copy can be found here. There are 35 treatment centers in Texas for early treatment of COVID and if you need help finding one near you, there is a link to a list within this guide. As a society, we need to be questioning the radical suppression of early treatment options for a potentially fatal virus. It simply makes no logical sense.
.
Heliobas Disciple
TB Fanatic
Posting this also from Profit of Doom
voiceforscienceandsolidarity.substack.com
(fair use applies)
VSS Science Updates During Pandemic Times #7
Geert Vanden Bossche
Mar 7 2022
Goal: Our newsletter aims at providing regular updates on the science and the truth behind the current pandemic. We are dedicated to bringing the real science to the table and sharing how the truth invalidates the current narrative, for which scientific evidence is now increasingly lacking. We’ll provide an update on a (semi-)weekly basis, on Mondays and/or Fridays. We sincerely hope this newsletter will contribute to raising awareness about the consequences of human intervention in this pandemic, particularly of mass vaccination, from both an individual and public health perspective.
1. UK Gov Releases Report Confirming the Fully Vaccinated Account For 9 in Every 10 Covid Deaths in England
“The latest data published by the UK Health Security Agency confirms deaths are rising dramatically among the triple vaccinated population whilst declining steadily among the not-vaccinated population in England.”
Whilst you've been distracted by Russia's Invasion, the UK Gov. released a Report confirming the Fully Vaccinated now account for 9 in every 10 Covid-19 Deaths in England
2. New Short Film: A Letter to Andrew Hill
In October 2020 Dr Andrew Hill was tasked to report to the World Health Organisation on the dozens of new studies from around the world suggesting that Ivermectin could be a remarkably safe and effective treatment for COVID-19. In the end, Dr Hill advised that “Ivermectin should be validated in larger appropriately controlled randomized trials before the results are sufficient for review by regulatory authorities.” What were his reasons for doing so? Were his conclusions justified? Or were external forces influencing his about-face?
A Letter to Andrew Hill | Oracle Films
3. Ivermectin May Help Prevent SARS-CoV-2 Conversion of M1 LB- Foamy Macrophages to M2 LB+ Foamy Macrophages
“Thus, ivermectin may not only reverse immunosenescence, but may also prevent early conversion of LB- FMs to LB+ FMs. This may help explain why ivermectin seems to synergize with Vitamin D, zinc and flavonoids in attenuating COVID-19 severity.”
HERV-K102 and Pandemic Responses
IVERMECTIN's Little Secret
Figure 1. The Ivermectin - SARS-CoV-2 String PPI Network Map Li N et al., 2021. In an effort to understand how ivermectin might protect against COVID-19 severity, Li N et al., 2021 derived a 52 protein-protein interaction (PPI) string network map …
Read more
8 days ago · 1 comment · Dr. Marian Laderoute
4. In the Omicron era, the Effectiveness Against Cases of BNT162b2 Declined Rapidly for Children
Effectiveness of the BNT162b2 vaccine among children 5-11 and 12-17 years in New York after the Emergence of the Omicron Variant
5. German Insurance Executive Fired Over Covid Vaccine Data Analysis
“It did not take long for the insurance executive, Andreas Schofbeck, who reported the extrapolation of 400,000 consultations, to be ‘dismissed without notice after a meeting of the board of directors’…"
Rounding the Earth Newsletter
German Insurance Executive Fired Over Quasi-Vaccine Data Analysis
The battle over open discussion of COVID-19 quasi-vaccine data gets uglier by the day. A few days ago I discussed the mortality estimates by German insurer BKK ProVita here: It did not take long for the insurance executive, Andreas Schofbeck, who reported the extrapolation of 400,000 consultations, to be …
Read more
6 days ago · 194 likes · 78 comments · Mathew Crawford
6. BioNTech Paid FDA $2,875,842.00 “Drug User Fee” for COVID-19 Vaccine Approval
Just Released Documents by Pfizer Show BioNTech Paid FDA $2,875,842.00 “Drug User Fee” for COVID-19 Vaccine Approval
7. The COVAX Delusion Reinforces Pharmaceutical Colonialism
“Mass vaccination of those at minimal risk, with a vaccine that does not reduce transmission, is poor public health practice.”
The COVAX Delusion Reinforces Pharmaceutical Colonialism ⋆ Brownstone Institute
.
VSS Science Updates During Pandemic Times #7
Goal: Our newsletter aims at providing regular updates on the science and the truth behind the current pandemic. We are dedicated to bringing the real science to the table and sharing how the truth invalidates the current narrative, for which scientific evidence is now increasingly lacking...
voiceforscienceandsolidarity.substack.com
VSS Science Updates During Pandemic Times #7
Geert Vanden Bossche
Mar 7 2022
Goal: Our newsletter aims at providing regular updates on the science and the truth behind the current pandemic. We are dedicated to bringing the real science to the table and sharing how the truth invalidates the current narrative, for which scientific evidence is now increasingly lacking. We’ll provide an update on a (semi-)weekly basis, on Mondays and/or Fridays. We sincerely hope this newsletter will contribute to raising awareness about the consequences of human intervention in this pandemic, particularly of mass vaccination, from both an individual and public health perspective.
1. UK Gov Releases Report Confirming the Fully Vaccinated Account For 9 in Every 10 Covid Deaths in England
“The latest data published by the UK Health Security Agency confirms deaths are rising dramatically among the triple vaccinated population whilst declining steadily among the not-vaccinated population in England.”
Whilst you've been distracted by Russia's Invasion, the UK Gov. released a Report confirming the Fully Vaccinated now account for 9 in every 10 Covid-19 Deaths in England
2. New Short Film: A Letter to Andrew Hill
In October 2020 Dr Andrew Hill was tasked to report to the World Health Organisation on the dozens of new studies from around the world suggesting that Ivermectin could be a remarkably safe and effective treatment for COVID-19. In the end, Dr Hill advised that “Ivermectin should be validated in larger appropriately controlled randomized trials before the results are sufficient for review by regulatory authorities.” What were his reasons for doing so? Were his conclusions justified? Or were external forces influencing his about-face?
A Letter to Andrew Hill | Oracle Films
3. Ivermectin May Help Prevent SARS-CoV-2 Conversion of M1 LB- Foamy Macrophages to M2 LB+ Foamy Macrophages
“Thus, ivermectin may not only reverse immunosenescence, but may also prevent early conversion of LB- FMs to LB+ FMs. This may help explain why ivermectin seems to synergize with Vitamin D, zinc and flavonoids in attenuating COVID-19 severity.”
HERV-K102 and Pandemic Responses
IVERMECTIN's Little Secret
Figure 1. The Ivermectin - SARS-CoV-2 String PPI Network Map Li N et al., 2021. In an effort to understand how ivermectin might protect against COVID-19 severity, Li N et al., 2021 derived a 52 protein-protein interaction (PPI) string network map …
Read more
8 days ago · 1 comment · Dr. Marian Laderoute
4. In the Omicron era, the Effectiveness Against Cases of BNT162b2 Declined Rapidly for Children
Effectiveness of the BNT162b2 vaccine among children 5-11 and 12-17 years in New York after the Emergence of the Omicron Variant
5. German Insurance Executive Fired Over Covid Vaccine Data Analysis
“It did not take long for the insurance executive, Andreas Schofbeck, who reported the extrapolation of 400,000 consultations, to be ‘dismissed without notice after a meeting of the board of directors’…"
Rounding the Earth Newsletter
German Insurance Executive Fired Over Quasi-Vaccine Data Analysis
The battle over open discussion of COVID-19 quasi-vaccine data gets uglier by the day. A few days ago I discussed the mortality estimates by German insurer BKK ProVita here: It did not take long for the insurance executive, Andreas Schofbeck, who reported the extrapolation of 400,000 consultations, to be …
Read more
6 days ago · 194 likes · 78 comments · Mathew Crawford
6. BioNTech Paid FDA $2,875,842.00 “Drug User Fee” for COVID-19 Vaccine Approval
Just Released Documents by Pfizer Show BioNTech Paid FDA $2,875,842.00 “Drug User Fee” for COVID-19 Vaccine Approval
7. The COVAX Delusion Reinforces Pharmaceutical Colonialism
“Mass vaccination of those at minimal risk, with a vaccine that does not reduce transmission, is poor public health practice.”
The COVAX Delusion Reinforces Pharmaceutical Colonialism ⋆ Brownstone Institute
.
Last edited:
Heliobas Disciple
TB Fanatic
Another one from Profit of Doom:
boriquagato.substack.com
(fair use applies)
homogenizing herd level antigenic fixation
why covid vaccine driven OAS may be much more dangerous than what we have seen in flu
el gato malo
17 hrs ago
antigenic fixation is a well studied issue, especially around influenza. how it came to have the oddly religion invoking name of “original antigenic sin” (OAS) is anyone’s guess, but it probably gives you some sense of how long this field of study has been going on.
i have spent a fair bit of time looking at it from the individual level and as a process mediated and accelerated by covid vaccines.
i think we’re well past the preponderance of evidence standard here and have strong reason to believe that covid vaccines have led to omicron as an OAS variant by creating an evolutionary gradient that selected for it.
but there are some reasons to be particularly worried about how this will affect the future at a societal/herd immunity level that we have not explored and i think we need to, because this antigenic fixation generated by the widespread application of a badly leaky or even infection amplifying vaccine is quite different that what occurs in nature.
most OAS is natural. it’s juts a property of human immune function in the face of pathogens that mutate a lot. we have seen this same thing in flu. you build up a set of immune responses when you are young and fixate into them.
as you get old and your generalized responses attenuate, you rely upon these learned responses more and more. old age and experience substitutes for for youth and a potent army of generalized immune responders. this is expected and normal.
then, one day, a variant comes along that is similar enough to something you had in the past to trigger the old response but different enough to render that response ineffective.
and suddenly, flu is very dangerous for you. you’re relying upon an ineffective antibody and cannot compensate with a robust generalized response. this is a big part of why flu gets so high risk for the elderly.
but from a herd standpoint, this is not a terribly dangerous issue.
it has limited overall social effects as the fixations of each person are widely varied and depend upon what pathogens they were exposed to in the past. this heterogeneity of herd immune characteristics prevents strong selectors for far reaching OAS variants from emerging.
and this is a VERY important concept.
everyone gets some degree of OAS for influenza. but we get different OAS because we had different exposures when we were young. it was different flus in different places and different times. the imprinting is polyglot therefore the herd has a heterogeneous immunity structure.
this means that when some new viral mutation or throwback finds consonance with a certain kind of imprinted immunity and preys upon OAS, the effects are limited to small groups.
this keeps large risks firewalled and prevents pandemics. flu sort of settles in to a long term average because you are, in effect, rolling lots and lots of small stakes dice all the time. you always lose a certain number of rolls, but they don’t clean you out. you get predictable outcomes within predictable standard deviations.
but in a situation like this where 70-90% of populations ALL got the same narrow inoculum exposure from a leaky (non-sterilizing) vaccine, that's not going to be the case. fixation is homogenous. everyone’s immune system pony has been taught the same one trick.
this may have very serious implications.
clearly, i am starting to speculate and extrapolate here. i’m not sure anything like this setup has every happened in humans before. these are going to be some scary questions and concepts. i’m not trying to run around like chicken little or over-amplify the risk, but i also think this needs to be elevated to the realm of serious discussion.
so, i’m going to lay out these hypotheses as best i can given the key salients as i understand them and and try to thread the needle between getting to the marrow of the issue and veering into unsubstantiated fear narratives rooted in corner cases.
so let’s think about what it means if we have a large segment that are immuno-fixated in identical fashion with a non-sterilizing inoculum:
foremost, it means that now if there is a mutation that finds a way to take advantage of this specific fixation it has a HUGE cohort to infect.
what might previously have been 2-5% of population at risk is now 70-90%. and that changes everything. now, one bad throw of the evolutionary dice and you have an instant pandemic where none was possible before.
welcome to the high stakes covidian crapshoot.
now buckle up, because this gets much, much worse:
the dice in this game are loaded.
you saw how quickly omicron chased the vaccination campaigns. my strong suspicion is that this was not a coincidence. it was driven BY the selective pressure of the vaccines that took what looks to be a throwback variant that did not evolve from delta but rather diverged from it all the way back at the original pre-alpha ancestor and surged it to sudden global prominence.
omicron is so divergent from other SARS-COV2 variants that some are arguing (HERE in “nature”) that it constitutes an entirely different serotype. (bold mine)
but it is precisely such variants that a society of homogeneously immuno-fixated hosts selects for.
if you have a large pool of hosts that all have the same fixation, then you have a large number of individual labs in which to have such a mutation occur.
the emergence of such variants is inherently a function of underlying mutation rate of the virus (which is high in covid strains) times the number of potential hosts and if the “win” state for virus is the same in all those hosts, then, in effect, all the labs are working on the same problem. you’ve effectively crowd sourced it to 70-90% of the population.
then some mutation chances on a high replication strategy and it goes like wildfire because so many are similarly susceptible.
so you you get a sort of “perfect storm.”
you have far more hosts in which to have random chances occur, all selecting for a mutation that attacks one specific weakness and that weakness is in most of the population, so once it’s out, there is no stopping it.
ouch.
and if this fixation prevents the hosts from developing strong new immunities based on these novel pathogens, this becomes iterative. you get wave after wave of pandemics until you wipe out the susceptible population.
boosters won’t help, they certainly have not so far. they may well make it worse and drive further fixation. you really cannot live in a constantly immuno-activated state in any event. it’s not good for you and the side and adverse effects will really pile up.
new vaccines may not work either. if an actual pathogen cannot drive immune adaptation, there is little reason to suspect that a vaccine can.
this could be a devilish issue with no solution that seems obvious (at least to me).
so let’s once more be clear: there is a lot here that we still do not know and this is not a proven hypothesis, but this does appear a serious potential issue.
i’m not sure we’ve ever seen anything like it before in human evolutionary history.
this could be with us for for a long time and these pandemics will spread far faster and further than they would otherwise and make it into everyone’s problem, vaxxed or not.
obviously, the public health irony of that one would be unspeakable. (though not unpredicted…)
it’s possible i’m wrong and this OAS issue will fade, but i hesitate to bet on it. generally, once you get this sort of strong response lock, you keep it. beta cells are forever.
it’s possible i’m wrong and that there will be cross immunities to other covids that will help and provide sufficient heterogeneity to act as firebreaks and generate enough functional heterogeneity to short circuit this, but given the way that omicron spread and the manner in which N-antibody immunity development looks suppressed by vaccines, this seems like a difficult bet to rely on.
it’s possible there is all sorts of stuff i missed and have failed to consider here. so let’s keep in mind we’re dealing in hypotheticals and that this is just one feline’s opinion.
honestly, i hope i’m wrong. the public health and public policy implications of this are draconian and dire.
it means we’ll get to play “covid pandemic” over and over with the same agencies and tyrants grasping for power and purpose and with a permanent class of carriers who are going to bear a nasty brunt and share it with the rest of us.
but it looks plausible to me and worthy of discussion. it fits the facts as they appear to me. it’s unpleasant, no one wants to hear it, but truths do not stop being true just because they are hard truths and not all monsters go back in the closet if you ignore them.
or perhaps it’s no monster at all.
so have at it. dispute this and prove me wrong. honestly, i’d be grateful because this is not an outcome anyone wants and i would flat out sleep better if i saw the error in this thinking.
or perhaps someone has a solution i have not considered. rule one of not being able to solve a problem is “show it to more people.” so more eyes are good.
we are, all in this together. so, maybe we could try acting like it. it can’t be worse than what we’ve done on covid so far…
.
homogenizing herd level antigenic fixation
why covid vaccine driven OAS may be much more dangerous than what we have seen in flu
boriquagato.substack.com
homogenizing herd level antigenic fixation
why covid vaccine driven OAS may be much more dangerous than what we have seen in flu
el gato malo
17 hrs ago
antigenic fixation is a well studied issue, especially around influenza. how it came to have the oddly religion invoking name of “original antigenic sin” (OAS) is anyone’s guess, but it probably gives you some sense of how long this field of study has been going on.
i have spent a fair bit of time looking at it from the individual level and as a process mediated and accelerated by covid vaccines.
i think we’re well past the preponderance of evidence standard here and have strong reason to believe that covid vaccines have led to omicron as an OAS variant by creating an evolutionary gradient that selected for it.
but there are some reasons to be particularly worried about how this will affect the future at a societal/herd immunity level that we have not explored and i think we need to, because this antigenic fixation generated by the widespread application of a badly leaky or even infection amplifying vaccine is quite different that what occurs in nature.
most OAS is natural. it’s juts a property of human immune function in the face of pathogens that mutate a lot. we have seen this same thing in flu. you build up a set of immune responses when you are young and fixate into them.
as you get old and your generalized responses attenuate, you rely upon these learned responses more and more. old age and experience substitutes for for youth and a potent army of generalized immune responders. this is expected and normal.
then, one day, a variant comes along that is similar enough to something you had in the past to trigger the old response but different enough to render that response ineffective.
and suddenly, flu is very dangerous for you. you’re relying upon an ineffective antibody and cannot compensate with a robust generalized response. this is a big part of why flu gets so high risk for the elderly.
but from a herd standpoint, this is not a terribly dangerous issue.
it has limited overall social effects as the fixations of each person are widely varied and depend upon what pathogens they were exposed to in the past. this heterogeneity of herd immune characteristics prevents strong selectors for far reaching OAS variants from emerging.
and this is a VERY important concept.
everyone gets some degree of OAS for influenza. but we get different OAS because we had different exposures when we were young. it was different flus in different places and different times. the imprinting is polyglot therefore the herd has a heterogeneous immunity structure.
this means that when some new viral mutation or throwback finds consonance with a certain kind of imprinted immunity and preys upon OAS, the effects are limited to small groups.
this keeps large risks firewalled and prevents pandemics. flu sort of settles in to a long term average because you are, in effect, rolling lots and lots of small stakes dice all the time. you always lose a certain number of rolls, but they don’t clean you out. you get predictable outcomes within predictable standard deviations.
but in a situation like this where 70-90% of populations ALL got the same narrow inoculum exposure from a leaky (non-sterilizing) vaccine, that's not going to be the case. fixation is homogenous. everyone’s immune system pony has been taught the same one trick.
this may have very serious implications.
clearly, i am starting to speculate and extrapolate here. i’m not sure anything like this setup has every happened in humans before. these are going to be some scary questions and concepts. i’m not trying to run around like chicken little or over-amplify the risk, but i also think this needs to be elevated to the realm of serious discussion.
so, i’m going to lay out these hypotheses as best i can given the key salients as i understand them and and try to thread the needle between getting to the marrow of the issue and veering into unsubstantiated fear narratives rooted in corner cases.
so let’s think about what it means if we have a large segment that are immuno-fixated in identical fashion with a non-sterilizing inoculum:
foremost, it means that now if there is a mutation that finds a way to take advantage of this specific fixation it has a HUGE cohort to infect.
what might previously have been 2-5% of population at risk is now 70-90%. and that changes everything. now, one bad throw of the evolutionary dice and you have an instant pandemic where none was possible before.
welcome to the high stakes covidian crapshoot.
now buckle up, because this gets much, much worse:
the dice in this game are loaded.
you saw how quickly omicron chased the vaccination campaigns. my strong suspicion is that this was not a coincidence. it was driven BY the selective pressure of the vaccines that took what looks to be a throwback variant that did not evolve from delta but rather diverged from it all the way back at the original pre-alpha ancestor and surged it to sudden global prominence.
omicron is so divergent from other SARS-COV2 variants that some are arguing (HERE in “nature”) that it constitutes an entirely different serotype. (bold mine)
The magnitude of immune evasion of Omicron raises the question whether it should be considered as a distinct SARS-CoV-2 serotype. Here, we discuss lines of evidence in support or against the concept of SARS-CoV-2 serotypes, and the implications of this classification…..
Antigenic cartography analyses indicated that all VOCs except Omicron belong to one large antigenic cluster, whereas Omicron forms a new cluster, escaping vaccine or convalescent sera7,8.
but it is precisely such variants that a society of homogeneously immuno-fixated hosts selects for.
if you have a large pool of hosts that all have the same fixation, then you have a large number of individual labs in which to have such a mutation occur.
the emergence of such variants is inherently a function of underlying mutation rate of the virus (which is high in covid strains) times the number of potential hosts and if the “win” state for virus is the same in all those hosts, then, in effect, all the labs are working on the same problem. you’ve effectively crowd sourced it to 70-90% of the population.
then some mutation chances on a high replication strategy and it goes like wildfire because so many are similarly susceptible.
so you you get a sort of “perfect storm.”
you have far more hosts in which to have random chances occur, all selecting for a mutation that attacks one specific weakness and that weakness is in most of the population, so once it’s out, there is no stopping it.
ouch.
and if this fixation prevents the hosts from developing strong new immunities based on these novel pathogens, this becomes iterative. you get wave after wave of pandemics until you wipe out the susceptible population.
boosters won’t help, they certainly have not so far. they may well make it worse and drive further fixation. you really cannot live in a constantly immuno-activated state in any event. it’s not good for you and the side and adverse effects will really pile up.
new vaccines may not work either. if an actual pathogen cannot drive immune adaptation, there is little reason to suspect that a vaccine can.
this could be a devilish issue with no solution that seems obvious (at least to me).
so let’s once more be clear: there is a lot here that we still do not know and this is not a proven hypothesis, but this does appear a serious potential issue.
i’m not sure we’ve ever seen anything like it before in human evolutionary history.
this could be with us for for a long time and these pandemics will spread far faster and further than they would otherwise and make it into everyone’s problem, vaxxed or not.
obviously, the public health irony of that one would be unspeakable. (though not unpredicted…)
it’s possible i’m wrong and this OAS issue will fade, but i hesitate to bet on it. generally, once you get this sort of strong response lock, you keep it. beta cells are forever.
it’s possible i’m wrong and that there will be cross immunities to other covids that will help and provide sufficient heterogeneity to act as firebreaks and generate enough functional heterogeneity to short circuit this, but given the way that omicron spread and the manner in which N-antibody immunity development looks suppressed by vaccines, this seems like a difficult bet to rely on.
it’s possible there is all sorts of stuff i missed and have failed to consider here. so let’s keep in mind we’re dealing in hypotheticals and that this is just one feline’s opinion.
honestly, i hope i’m wrong. the public health and public policy implications of this are draconian and dire.
it means we’ll get to play “covid pandemic” over and over with the same agencies and tyrants grasping for power and purpose and with a permanent class of carriers who are going to bear a nasty brunt and share it with the rest of us.
but it looks plausible to me and worthy of discussion. it fits the facts as they appear to me. it’s unpleasant, no one wants to hear it, but truths do not stop being true just because they are hard truths and not all monsters go back in the closet if you ignore them.
or perhaps it’s no monster at all.
so have at it. dispute this and prove me wrong. honestly, i’d be grateful because this is not an outcome anyone wants and i would flat out sleep better if i saw the error in this thinking.
or perhaps someone has a solution i have not considered. rule one of not being able to solve a problem is “show it to more people.” so more eyes are good.
we are, all in this together. so, maybe we could try acting like it. it can’t be worse than what we’ve done on covid so far…
.