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New tool aids in early detection of COVID variants
by American Museum of Natural History
October 29, 2024

Researchers have demonstrated a new technique for COVID surveillance that can signal the rise of new variants before they are widespread. The study, led by the American Museum of Natural History and Columbia University and published in the journal Genome Research, presents a way to track diversity across millions of genomes sequenced during the height of the COVID-19 pandemic using new surveillance software and points to its potential use in future pandemics.

During the COVID-19 pandemic, researchers all over the world used analyses of genomic data to guide policy. Sequences of SARS-CoV-2, the virus that causes COVID-19, revealed rapid evolution of new strains that were more contagious or more severe than the original virus.

"The architecture of the COVID-19 pandemic is marked by periods of transition, tipping a population towards an emerging variant of concern, followed by its near complete sweep to dominance," said Apurva Narechania, lead author of the new study and a senior bioinformaticist at the Museum's Institute for Comparative Genomics. "Speed is key to responding to these evolving strains, but the traditional way of analyzing these sequences slows down surveillance techniques."

Working closely with colleagues in public health, Narechania looked at long-standing definitions of diversity that are used in ecology. In particular, the research team focused on Hill numbers, or the effective number of species in a sample, which provides a simple metric for comparing species diversity across environments. The more diverse the sample, the higher the Hill number. The new pandemic surveillance software developed by the American Museum of Natural History-Columbia University team adopts this ecological approach, but in the place of species, the researchers use strings of sequence information, and in the place of environments, they use genomes.

The researchers tested this software on COVID-19 sequence data from multiple countries, including the United Kingdom, United States, and South Africa, finding that it accurately predicts the arc of variant emergence before the onset of sickness in the population.

"The viral surveillance we had during COVID-19 was a few weeks to months behind the edge of the pandemic curve," said Barun Mathema, an associate professor of epidemiology at Columbia University's Mailman School of Public Health and a corresponding author on the study. "In a crisis of COVID-19's scale and speed, eliminating this analysis lag can mean the difference between timely, reasonable public health response and failure to understand and anticipate the disease's next turn."

The software, now on GitHub, and freely available to non-commercial entities, cannot characterize new variants, but it can forewarn public health officials when a new strain is on the horizon and signal when more in-depth bioinformatics tools are needed. The researchers point to the software's ability to detect new variants in wastewater as a particularly impactful potential application.

"We show that tracing a pandemic curve with these new metrics enables the use of sequence data as a real-time sensor, tracking both the emergence of variants over time and the extent of their spread," Mathema said. "Our technique affords public health institutions the opportunity to create actionable policy based on a simple, quantitative measure."

Narechania didn't originally set out to solve this particular disease surveillance issue. The project began in 2020 with a focus on bacteria, which--like viruses--can be very difficult to map onto an evolutionary tree.

"I don't think I would have had this idea if I didn't work at the Museum," he said. "The original intent was to reimagine how we understand microbial species, but after COVID emerged, we turned our attention to tracing the pandemic's natural history and testing whether it could be an effective tool in disease monitoring. The answer was a resounding yes."

Other authors on the paper include Dean Bobo, American Museum of Natural History and Columbia University; Kevin Deitz and Rob Desalle, American Museum of Natural History; and Paul Planet, American Museum of Natural History, Children's Hospital of Pennsylvania, and the University of Pennsylvania.

More information: Apurva Narechania et al, Rapid SARS-CoV-2 surveillance using clinical, pooled, or wastewater sequence as a sensor for population change, Genome Research (2024). DOI: 10.1101/gr.278594.123
Journal information: Genome Research
Provided by American Museum of Natural History
 

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How COVID-19 Revitalized Family Dinners
By American Psychological Association
October 31, 2024

The pandemic saw families eating together more often, with dinners marked by increased positivity and connectivity, aided by technology that brought distant family members closer.

The COVID-19 lockdowns led to more frequent and quality-rich family dinners, enhancing positive interactions among family members.

The use of technology for remote dining with extended family members increased, possibly sustaining these new family dynamics post-pandemic.


Pandemic Impact on Family Meals

During the COVID-19 lockdowns, many families found themselves eating more meals at home. According to research from the American Psychological Association, this shift had an unexpected benefit: it increased the quality of family time during meals.

The study, featured in the journal Couple and Family Psychology: Research and Practice, revealed that families who dined together more frequently during the pandemic also enjoyed more positive interactions. They shared news and information, and many used technology, like videoconferencing, to stay connected with family members who lived far away.

“The predominance of past research on family dinners has focused on frequency as the key predictor of benefits for children and adolescents,” explained lead author Anne Fishel, PhD, a clinician and family therapy researcher at Massachusetts General Hospital. “This study highlights the importance of examining both frequency and quality to understand the full picture of how shared meals can impact families.”


Enhanced Family Interactions

Researchers examined data from a survey of 517 ethnically and socioeconomically diverse parents across the United States, administered in May 2021. Their aim was to investigate changes in family dinner frequency and quality during the COVID-19 pandemic.

Participants were asked about dinner frequency, quality, and post-pandemic expectations. The survey included questions about positive and negative interactions, family support, and incorporation of the outside world. They were asked questions such as, “During the pandemic, did all or most of the people living in your home eat dinner together less, about the same, or more than compared to before the pandemic?” Participants then provided answers ranging on a scale of 1-5, 1 being “much less” and 5 being “much more.”

Over 60% of respondents reported eating dinner together more often during the pandemic compared with pre-pandemic times. There was also a significant increase in positive interactions (e.g, expressing gratitude, laughing or feeling connected) during family meals.

“Specifically, 56% said they increased talking about their days during dinner, 60% said they increased talking about their identity as a family, 60% said they increased expressing gratitude, 67% said they increased laughing together and 59% said they felt more connected to each other around the dinner table,” said Fishel. This positive association was evident across income levels, education, age, gender, and race.


Role of Technology in Family Dinners

The pandemic introduced new aspects to family dinners, including remote dining with extended family members and more discussions about current events, according to Fishel. Many families turned to videoconferencing to connect with extended family, potentially strengthening a sense of belonging to a larger family unit. Most parents who increased the use of technology for remote dinners during the pandemic reported that they plan to continue this practice as the pandemic subsides.

The researchers also found an increase in families incorporating news and information from the outside world into their dinner conversations, potentially offering a safe space for children to discuss anxieties and questions with their parents.


Lasting Positive Effects on Family Dynamics

Overall, this study suggests that the increased frequency of family dinners during the pandemic may have had lasting positive effects on family dynamics, according to Fishel.

“The pandemic changed many aspects of our lives, some for the better. Even though parents did not purposely sign up to have more shared mealtimes, increases in family dinners were largely linked with improvements in the quality of pandemic-era family dinners,” she said.

The findings also highlight the potential benefits of using technology to connect with extended family and incorporating current events into dinner conversations.

“The continued use of remote technology to connect with those not physically present may bring ongoing opportunities for family bonding and children’s feeling a sense of belonging to a larger unit, which we know is protective for their well-being,” said Fishel.

Reference: “How COVID-19 expanded the family dinner table: Greater frequency linked with improved quality and new ways of eating together” by Anne Fishel, PhD and Melinda I. Morrill, PhD, 31 October 2024, Couple and Family Psychology: Research and Practice.
DOI: 10.1037/cfp0000268
 

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Risk of post-COVID symptoms linked to body mass index in children
by Justin Jackson , Medical Xpress
October 31, 2024 report

A study by the University of Pennsylvania and researchers from 26 U.S. children's hospitals has linked elevated body mass index (BMI) to a significantly higher risk of developing post-acute sequelae of SARS-CoV-2 infection (PASC) among children and young adults.

The study revealed a 25.4% increased risk of PASC among those with obesity and a 42.1% increased risk among those with severe obesity compared to peers with a healthy BMI.

PASC encompasses a wide range of persistent, relapsing, or newly emerging symptoms that last beyond four weeks after the acute phase of COVID-19. According to the NIH, the most common signs and symptoms are fatigue, shortness of breath, muscle pain, joint pain, headache, cough, chest pain, altered smell, altered taste, and diarrhea.

The study additionally identifies many more symptoms, such as abdominal pain, abnormal liver enzyme levels, acute kidney injury, acute respiratory distress syndrome, arrhythmias, cognitive dysfunction, fever and chills, fluid and electrolyte imbalances, generalized pain, hair loss, heart disease, mental health disorders, myocarditis, myositis, postural orthostatic tachycardia syndrome (POTS) or dysautonomia, skin symptoms, thrombophlebitis, and thromboembolism.

While obesity is known to be associated with increased severity of COVID-19, its relationship with PASC in pediatric populations has been unclear.

In a retrospective cohort study, "Body Mass Index and Postacute Sequelae of SARS-CoV-2 Infection in Children and Young Adults," published in JAMA Network Open, the researchers looked for trends correlating to body mass in PASC.

The team analyzed data from 172,136 participants aged 5 to 20 with documented SARS-CoV-2 infection between March 2020 and May 2023. Participants were categorized based on their BMI status prior to infection: healthy weight, overweight, obesity, and severe obesity.

Results showed that compared with participants with a healthy weight, those with obesity had a 25.4% increased risk of PASC. Those with severe obesity had a 42.1% increased risk when identified using the diagnostic code for post–COVID–19 conditions. An increased risk for any occurrences of PASC symptoms and conditions was also observed among those with obesity and severe obesity.

The researchers concluded that elevated BMI is associated with a significantly increased PASC risk in a dose-dependent manner, highlighting the need for targeted care to prevent chronic conditions in at-risk children and young adults.

More information: Ting Zhou et al, Body Mass Index and Postacute Sequelae of SARS-CoV-2 Infection in Children and Young Adults, JAMA Network Open (2024). DOI: 10.1001/jamanetworkopen.2024.41970
Journal information: JAMA Network Open
 

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German Study Finds That Emerging COVID-19 Variants Show Strong Resistance to Antibodies and Heightrned Cell Entry

Nikhil Prasad Fact checked by:Thailand Medical News Team
Nov 01, 2024

Researchers from top German research institutions have conducted an in-depth analysis of the latest SARS-CoV-2 variants, KP.2, KP.2.3, KP.3, and LB.1, uncovering a powerful potential for these lineages to evade antibodies generated by previous infections and vaccines. This study highlights how these variants have evolved to increase their efficiency in entering human cells and avoiding immune defenses.

The research team includes experts from the German Primate Center–Leibniz Institute for Primate Research, Georg-August-University Göttingen, Friedrich-Alexander University of Erlangen-Nürnberg, Hannover Medical School, and the German Centre for Infection Research.


Higher Efficiency in Host Cell Entry
The study used pseudotyped particles to analyze how efficiently these variants could enter various human cells. This Medical News report delves into findings that KP.2, KP.2.3, KP.3, and LB.1 have shown high adaptability, demonstrating that the mutations in these strains allow them to enter cells at higher or comparable rates to the JN.1 strain, which had previously dominated global COVID-19 cases. Among these variants, KP.3 showed the highest entry efficiency into lung cells, especially Calu-3 lung cells, a type of human cell particularly vulnerable to severe infection.


Different Ways of Utilizing ACE2 Receptors

The researchers noted subtle differences in how these variants bind to the ACE2 receptor, the main protein SARS-CoV-2 uses to enter human cells. KP.2, for example, was capable of using both human and murine ACE2 receptors effectively, whereas KP.2.3 and LB.1 did not. This specificity might influence which animals, aside from humans, could be susceptible to infections with these variants, which could have implications for cross-species transmissions in the future.


Antibody Resistance: A Major Concern
One of the most concerning findings is that the variants KP.2, KP.2.3, KP.3, and LB.1 are highly resistant to antibody neutralization. The study tested several monoclonal antibodies, and only one, BD55-5514, managed to effectively neutralize all the variants. Others, such as BD56-1854 and Omi-42, displayed significantly reduced efficacy, highlighting a gap in the current antibody treatments available. This breakthrough discovery shows that these newer variants may be harder to neutralize even with existing therapeutic options, particularly for individuals who have not achieved “hybrid immunity” through both infection and vaccination.


Reduced Efficiency in Cell Fusion
Interestingly, the researchers also found that KP.2, KP.2.3, KP.3, and LB.1 variants led to less cell-to-cell fusion compared to the JN.1 strain. Cell fusion is a process where infected cells merge with neighboring healthy cells, contributing to the spread of the virus within the body. The lower fusion potential may imply a difference in how the virus spreads within the host but does not detract from its overall infectivity or immune evasion.


How These Variants Compare Globally

The study revealed that the older JN.1 variant is losing its prevalence worldwide, as KP.2, KP.2.3, and KP.3 become more common, indicating that these variants' unique mutations may help them spread more effectively. These findings are based on data gathered from samples between April and July 2024, which showed an upward trend for these newer lineages in several regions.


Key Mutations in Spike Proteins

Researchers examined mutations in the spike (S) protein of these variants, which allow them to bind more effectively to receptors on human cells and evade immune detection. The mutations, including R346T and F456L, play a significant role in enabling antibody resistance. The study also explored how these mutations impact the virus's ability to evade antibodies generated by the latest vaccine boosters adapted to the XBB.1.5 lineage, widely administered in response to earlier Omicron waves.


Conclusions

This study suggests that the adaptability of SARS-CoV-2 continues to challenge both natural and vaccine-induced immunity. The KP.2, KP.2.3, KP.3, and LB.1 variants pose an increased risk of infection due to their heightened cell entry efficiency and notable antibody resistance. The variations in ACE2 receptor usage could also indicate potential shifts in cross-species transmission risk. As current therapeutic monoclonal antibodies show limited efficacy against these new variants, the findings underscore the critical need for broad-spectrum antibodies and vaccines that can address this rapid viral evolution.

The study findings were published in the peer-reviewed journal: Vaccines.

 

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An Idaho health department isn't allowed to give COVID-19 vaccines anymore. Experts say it's a first
Devi Shastri
Updated Fri, November 1, 2024 at 6:36 PM UTC

A regional public health department in Idaho is no longer providing COVID-19 vaccines to residents in six counties after a narrow decision by its board.

Southwest District Health appears to be the first in the nation to be restricted from giving COVID-19 vaccines. Vaccinations are an essential function of a public health department.

While policymakers in Texas banned health departments from promoting COVID vaccines and Florida's surgeon general bucked medical consensus to recommend against the vaccine, governmental bodies across the country haven't blocked the vaccines outright.

“I'm not aware of anything else like this,” said Adriane Casalotti, chief of government and public affairs for the National Association of County and City Health Officials. She said health departments have stopped offering the vaccine because of cost or low demand, but not based on “a judgment of the medical product itself.”

The six-county district along the Idaho-Oregon border includes three counties in the Boise metropolitan area. Demand for COVID vaccines in the health district has declined — with 1,601 given in 2021 to 64 so far in 2024. The same is true for other vaccines: Idaho has the highest childhood vaccination exemption rate in the nation, and last year, the Southwest District Health Department rushed to contain a rare measles outbreak that sickened 10.

On Oct. 22, the health department’s board voted 4-3 in favor of the ban — despite Southwest's medical director testifying to the vaccine's necessity.

“Our request of the board is that we would be able to carry and offer those (vaccines), recognizing that we always have these discussions of risks and benefits,” Dr. Perry Jansen said at the meeting. “This is not a blind, everybody-gets-a-shot approach. This is a thoughtful approach.”

Opposite Jansen's plea were more than 290 public comments, many of which called for an end to vaccine mandates or taxpayer funding of the vaccines, neither of which are happening in the district. At the meeting, many people who spoke are nationally known for making the rounds to testify against COVID vaccines, including Dr. Peter McCullough, a Texas cardiologist who sells “contagion emergency kits” that include ivermectin and hydroxychloroquine — drugs that have not been approved to treat COVID-19 and can have dangerous side effects.

Board Chairman Kelly Aberasturi was familiar with many of the voices who wanted the ban, especially from earlier local protests of pandemic measures.

Aberasturi, who told The Associated Press that he's skeptical of COVID-19 vaccines and national public health leaders, said in the meeting and in an interview with the AP that he was supportive of but “disappointed” in the board's decision.

He said the board had overstepped the relationship between patients and their doctors — and possibly opened a door to blocking other vaccines or treatments.

Board members in favor of the decision argued people can get vaccinated elsewhere, and that providing the shots was equivalent to signing off on their safety. (Some people may be reluctant to get vaccinated or boosted because of misinformation about the shots despite evidence that they’re safe and have saved millions of lives.)

The people getting vaccinated at the health department — including people without housing, people who are homebound and those in long-term care facilities or in the immigration process — had no other options, Jansen and Aberasturi said.

“I’ve been homeless in my lifetime, so I understand how difficult it can be when you’re ... trying to get by and get ahead,” Aberasturi said. “This is where we should be stepping in and helping.

"But we have some board members who have never been there, so they don’t understand what it’s like.”

State health officials have said that they “recommend that people consider the COVID-19 vaccine.” Idaho health department spokesperson AJ McWhorter declined to comment on “public health district business,” but noted that COVID-19 vaccines are still available at community health centers for people who are uninsured.

Aberasturi said he plans to ask at the next board meeting if the health department can at least be allowed to vaccinate older patients and residents of long-term care facilities, adding that the board is supposed to be caring for the “health and well-being” of the district's residents. "But I believe the way we went about this thing is we didn't do that due diligence.”
 

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Michigan Supreme Court Dismisses COVID-19 Mandate Challenge
The court dismissed a challenge to COVID-19 mandates, leaving the state’s executive authority on future health restrictions unaddressed and intact.

By Tom Ozimek
11/1/2024

The Michigan Supreme Court has dismissed a case challenging the pandemic powers of the Michigan Department of Health and Human Services (DHHS), overturning a lower court’s finding the agency overstepped its authority with sweeping COVID-19 mandates.

By dismissing the case, the high court did not have to rule on the constitutionality of DHHS’s executive powers. It remains a question whether the department can impose similar restrictions on Michigan businesses and individuals in the future without legislative approval.

In a Nov. 1 order, the Michigan Supreme Court reversed part of a June 29, 2023 judgment of the Court of Appeals, ruling that the case is moot and vacating the remainder of the lower court’s opinion, which had determined that DHHS exceeded its authority with COVID-19 mandates like limiting public gatherings and mandating protective masks. In a 5–2 split decision, the high court ruled that the case should be declared moot because the mandates expired years ago and the plaintiff, River Crest Catering, has since closed its business.

Two dissenting justices, Richard H. Bernstein and David F. Viviano, argued that the appeals court’s finding—that DHHS overstepped its bound—was a “momentous ruling affecting the rights of all Michiganders” and should not be dismissed “so lightly.”

“While plaintiff has closed the doors to its physical catering business, the likelihood would appear to be significantly greater that other similar businesses might again be subject to restrictions similar to those issued during the COVID-19 pandemic,” wrote Viviano in dissent, joined by Bernstein.

The case, known as T & V Associates, Inc. v. Director of Health and Human Services, was brought by River Crest Catering, a Michigan business that argued COVID-19 restrictions imposed by DHHS in 2021 violated its rights. Specifically, River Crest contested a DHHS emergency order limiting gatherings at food service establishments, including outdoor ones, and requiring masks, claiming the agency’s mandate under a portion of Michigan’s Public Health Code (MCL 333.2253) infringed on its due process rights. The company sought a ruling to declare the order void and to challenge DHHS’s authority to impose such restrictions without legislative approval.

In April 2021, River Crest filed a complaint in the Court of Claims seeking a declaratory judgment, arguing that the section in the state’s public health code represented an unconstitutional delegation of legislative authority and that DHHS exceeded its authority under this statute. The plaintiff also claimed violations of its procedural and substantive due process rights.

In response, DHHS requested dismissal, asserting mootness, lack of standing, and failure to state a valid claim. The Court of Claims granted DHHS’s motion, concluding that while the case was not moot and River Crest had standing, the plaintiff failed to demonstrate an unconstitutional delegation of power and due process violations.

River Crest appealed the Court of Claims decision, and the Michigan Court of Appeals sided with the catering company in a split decision on June 29, 2023. The appellate court also found that the case was not moot, as the underlying legal issues—DHHS’s authority and the constitutionality of MCL 333.2253—remained relevant to businesses potentially facing similar mandates in future public health emergencies. Additionally, the Court of Appeals found that DHHS had overstepped its authority under the statute, marking a significant limitation on the agency’s ability to impose sweeping mandates without further legislative backing.

The Michigan Supreme Court’s Nov. 1 decision to overturn the appellate ruling and declare the case moot effectively removes the precedent set by the appellate court, meaning that DHHS’s authority under MCL 333.2253 remains largely undefined in terms of constitutional limits. This leaves Michigan state agencies with considerable discretion to interpret their emergency powers under the existing statute in the event of future health crises.

A request for comment on the implications of the ruling, sent to counsel representing River Crest in the case, was not immediately returned.
 

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Long COVID inflammation damages the heart, blood analysis finds

by University of Queensland
October 31, 2024

University of Queensland-led research has found inflammatory markers in the blood of long COVID patients which could explain why many experience ongoing cardiovascular issues.

Associate Professor Kirsty Short said the team set out to investigate the cause of persistent chest pain and heart palpitations commonly reported by many long COVID sufferers.

"We discovered elevated levels of cytokines, proteins which help control inflammation in the body, in the blood samples of people at about 18 months post-infection with SARS-CoV-2," Dr. Short said.

"Lab studies showed these trace-level cytokines had a direct effect on the functionality of cardiomyocytes, the cells of the heart responsible for its pump function.

"These particular types of cells are fundamental building blocks for our heart, so damaging them can lead to cardiovascular symptoms."

Dr. Short said until now, the role of chronic inflammation in cardiovascular symptoms hadn't been clear, particularly in individuals with symptoms persisting for over a year after infection.

The study, now published in Nature Microbiology, involved analyzing the blood of 50 participants across Australia who had either suffered long COVID for more than a year, had recovered from COVID, or had never had the virus.

The researchers used "immuno-storm chip" nanotechnology developed at UQ's Australian Institute for Bioengineering and Nanotechnology (AIBN) to discover trace elevated cytokines in the long COVID cohort, along with cardiac tissue damage markers measured at single-molecule resolution in blood.

"It's only early days and these results require validation in additional patient cohorts, including those infected with more recent SARS-CoV-2 strains," Dr. Short said.

"We're now curious to know whether our findings could be applied to other symptoms of long COVID such as neurological disease or respiratory disease, as this study actively recruited sufferers with chest pain and/or heart palpitations.

"Despite these limitations, this work offers some important new insights into this complex disease, and hopefully offers opportunities to improve the diagnosis, treatment and understanding of long COVID."

The research was led by UQ Ph.D. candidates Jane Sinclair from the School of Chemistry and Molecular Biosciences (SCMB), Courtney Vedelago from AIBN and Dr. Feargal J. Ryan from the South Australian Health and Medical Research Institute.

The research was a collaboration involving UQ's SCMB, School of Mathematics and Physics, AIBN, Institute for Molecular Bioscience and Faculty of Medicine as well as the South Australian Health and Medical Research Institute, Flinders University, the University of Adelaide, the Australian National University, Mater Health Queensland, Mater Research Institute—UQ and QIMR Berghofer Medical Research Institute.

The samples for the research were provided by the COVID OZGenetics study, the Central Adelaide Health Network and the David Serisier Research Biobank at Mater Research.

More information: Jane E. Sinclair et al, Post-acute sequelae of SARS-CoV-2 cardiovascular symptoms are associated with trace-level cytokines that affect cardiomyocyte function, Nature Microbiology (2024). DOI: 10.1038/s41564-024-01838-z
Journal information: Nature Microbiology
Provided by University of Queensland
 

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New model uses infection 'signatures' to predict who lives or dies of COVID-19
by Delthia Ricks , Medical Xpress
October 31, 2024


new-model-based-on-sig.jpg

Cellular infiltration and relationship of peripheral blood signatures and lung tissue lesions according to the disease trajectories leading to fatal outcome. Credit: Science Translational Medicine (2024). DOI: 10.1126/scitranslmed.adk9149

A critical challenge during the early COVID-19 pandemic was determining whether a patient would survive the infection or die from it. And even though a host of lifesaving therapeutics now spares substantially more lives than four years ago, the art of predicting COVID outcomes remains a matter of scientific pursuit.

Data from an international team of researchers in Scotland and Brazil suggest that their prediction model defines specific characteristics of SARS-CoV-2 infection that can be used to forecast disease outcomes and triage sick patients in hospitals.

The data in the new study are based on infections that occurred in 2020, and team members contend that their forecasting method is useful. But they worry that in 2024, patients' protection against COVID via vaccines could raise questions whether their method is a timely model. The study is published in the journal Science Translational Medicine.

Medical interventions that range from vaccines and antivirals to monoclonal antibodies have dramatically curtailed fatalities from COVID compared with the early years of the pandemic. Yet, the novel strategy, based on research involving patients in Brazil, reveals specific "signatures" of COVID infection, which allowed the team to forecast patients' outcomes with a fair degree of accuracy.

João Da Silva Filho of the Wellcome Center for Integrative Parasitology and the School of Infection and Immunity at University of Glasgow in Scotland has characterized and defined these signatures as they relate to specific stages of disease severity.

Working with collaborators at the University of Amazonas State and Federal University of Amazonas, both in in Manaus, Brazil, Da Silva Filho describes these stages as early death, late death, and recovery. The model can predict a patient's group upon admission to a hospital. The signatures of patients' infection determine their disease trajectory and fate, Da Silva Filho and colleagues say.

"COVID-19 is characterized by a broad range of symptoms and disease trajectories," Da Silva Filho writes in the article. "Understanding the correlation between clinical biomarkers and lung pathology during acute COVID-19 is necessary to understand its diverse pathogenesis and inform more effective treatments."

The signatures that Da Silva Filho and colleagues uncovered and say can be used to forecast COVID outcomes were derived from clinical and peripheral blood data gathered prior to and after the deaths of 142 COVID patients in Brazil. With respect to postmortem analysis, researchers examined lung tissues down to the single cell level to uncover specific signatures with lung-specific changes that Da Silva and collaborators say drive disease progression.

All 142 Brazilian patients studied in the analysis had been hospitalized for COVID. Da Silva Filho asserts that the findings can be used by other health care providers not only to triage COVID patients but to develop personalized treatments. Markers that determine disease signatures can be obtained in a blood test.

"We identified core clinical and peripheral blood signatures differentiating disease progression between patients who recovered from severe disease compared with those who succumbed to the disease," Da Silva Filho reported. "Signatures were heterogeneous among fatal cases yet clustered into two patient groups: early death, which referred to fewer than 15 days until death, and late death, which was more than 15 days until death.

"Progression to early death was characterized systemically and in lung histopathological samples by rapid endothelial and myeloid activation and the presence of thrombi associated with SARS-CoV-2+ macrophages," Da Silva Filho added.

Early death patients were characterized by a dysfunctional immune response, with intense vascular inflammation and clotting. The signature of late death patients was associated with fibrosis and programmed cell death—apoptosis—along with a delayed increase in interferon and the subset of T helper cells known as T helper cells 17, or simply TH17.

The analysis of postmortem lung tissue revealed distinct patterns of lung lesions related to disease progression, and distinct viral location in the lungs as the disease progressed to fatal outcomes.

Among patients whose biological signatures placed them in the "recovery" group had signatures that showed higher lymphocyte counts, more T helper 2 cell responses, and anti-inflammatory immune activity, the team found.

Despite the detail and the predictive value of the new data, the team of researchers says their study carries one huge caveat: Patients in the study were all admitted to hospitals during the earliest wave of the pandemic, between March and May of 2020.

"We do not know to what extent our findings would be applicable in the context of newer variants, and more importantly patients with a variable degree of background immunity provided by vaccination or previous infections," Da Silva Filho concluded.

More information: João Da Silva Filho et al, A spatially resolved single-cell lung atlas integrated with clinical and blood signatures distinguishes COVID-19 disease trajectories, Science Translational Medicine (2024). DOI: 10.1126/scitranslmed.adk9149
Journal information: Science Translational Medicine
 

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COVID-19 sharply boosts risk for blood-fat disorders, find researchers
by Albert Einstein College of Medicine
November 1, 2024


covid-19-sharply-boost.jpg

Monthly incidence of dyslipidemia in our population during the 6-year observation period. Credit: Journal of Clinical Investigation (2024). DOI: 10.1172/JCI183777

A study led by researchers at Albert Einstein College of Medicine involving more than 200,000 adults found that the COVID-19 pandemic caused a 29% increase in risk for developing dyslipidemia, a condition involving abnormal lipid (fat) levels in the blood.

Seniors and people with type 2 diabetes were even more strongly affected, experiencing an approximately two-fold increased risk for developing dyslipidemia, which is a major risk factor for cardiovascular diseases such as heart attack and stroke. The research was published today in the print edition of the Journal of Clinical Investigation.

"Given the extent of the pandemic, this increase in dyslipidemia risk is a cause for concern around the world," said study leader Gaetano Santulli, M.D., Ph.D., associate professor of medicine and of molecular pharmacology at Einstein. "Based on our findings, we would advise people to have their lipid levels monitored regularly and to consult with their health care providers about ways to treat dyslipidemia if detected, especially elderly individuals and patients with diabetes."

He noted that this advice would apply to all adults, not just those formally diagnosed with COVID-19, considering that many people have been infected without realizing it.

To put these findings into context, it has been estimated that 53% of U.S. adults had dyslipidemia before the pandemic; a 29% increase in dyslipidemia incidence due to COVID-19 would mean that 68% of Americans may now be at risk for having lipid abnormalities.

In two previous studies, Dr. Santulli and his team found that COVID-19 raised the incidence of new cases of hypertension and type 2 diabetes.

"In those analyses, we demonstrated that the risk of developing these disorders was still high three years after the pandemic; moreover, we noticed a suspicious increase in total cholesterol levels, which warranted a closer look," said Dr. Santulli.

In the new study, the researchers first determined the incidence of dyslipidemia in a group of more than 200,000 adults living in Naples, Italy, during the three years prior to the start of the pandemic (2017–2019). They then assessed the incidence of dyslipidemia in the same group during the three-year COVID-19 period (2020–2022), excluding from the analysis those people earlier diagnosed with dyslipidemia or who had previously been taking lipid-lowering medications.

The investigators found that COVID-19 raised the risk for developing dyslipidemia in the entire study group by an average of 29%. The increase was even higher among people over age 65 and those with chronic conditions, particularly diabetes and obesity, cardiovascular disease, chronic obstructive pulmonary disease, and hypertension.

The findings are the most definitive to date because other studies—most of them linking COVID-19 with modestly increased risks for blood-lipid problems—used as control groups different populations or people thought to have gone through the pandemic without becoming infected. However, significant numbers of people classified as "COVID-free" actually developed the disease but were either never tested or didn't seek medical care.

"Our study did not attempt to determine whether participants had tested positive for COVID-19," Dr. Santulli said. "Instead, because we had been following this group for many years prior to the pandemic, we were able to measure COVID's overall impact on the population by simply comparing levels of dyslipidemia in the same group before and after the pandemic. Any increase in dyslipidemia incidence would almost certainly have to be the result of COVID-19."

How COVID-19 might have increased the incidence of dyslipidemia remains unclear. One possible explanation is a finding Dr. Santulli made in an earlier study: that SARS-CoV-2 (the virus that causes COVID) disrupts the function of endothelial cells, which line the inside of blood vessels throughout the body and play a critical role in regulating blood lipids.

A separate study found that COVID-19 is a powerful risk factor for heart attacks and strokes for as long as nearly three years after an infection.

"This investigation, published online a month after ours, essentially confirms our observations in this study, since dyslipidemia is a major contributor to cardiovascular disease," said Dr. Santulli. "It also suggests that tackling dyslipidemia should reduce the risk of cardiovascular disease in those who have had COVID."

The researchers are now studying the effects of COVID-19 on cardiovascular-kidney-metabolic (CKM) syndrome, a recently described condition involving four connected medical problems—heart disease, kidney disease, diabetes, and obesity—all of which involve endothelial dysfunction.

More information: Valentina Trimarco et al, A six-year study in a real-world population reveals an increased incidence of dyslipidemia during COVID-19, Journal of Clinical Investigation (2024). DOI: 10.1172/JCI183777
Journal information: Journal of Clinical Investigation
Provided by Albert Einstein College of Medicine
 

Heliobas Disciple

TB Fanatic
Radagast just did a piece on bird flu today, I'll add it to go with that tweet. Keep in mind though he is a very strong proponent of vegetarianism which is evident in this piece.



(fair use applies)

What nobody wants to hear about bird flu
Radagast
November 3, 2024

Look, this is my blog, so I get to decide what I want to write about. I don’t have a bunch of fat American MAGA boomers sending me 5 dollars a month in exchange for telling them that Joe Biden’s climate change hysteria is going to make our meat and eggs expensive.

I look at this website a bit like my legacy. I will die one day and then I’ll be able to take comfort in the fact that I sought to tell people the truth, instead of the popular lie that makes you money. I don’t have to administer you addictive brain-opioids, that lull you to sleep. I get to tell you what you don’t want to hear. I get to tell you, the truth. People don’t lie to you to deceive you. They lie to you because you prefer being lied to.

But this is the truth and you’re not going to like it. The bird flu, is not “flu”. Yes, it’s technically an influenza virus, in the same sense as a bat is technically a mammal. But when you think of a mammal, you think of an animal that lives on land, not an animal that flies in the sky.

How many influenza viruses can you think of, that kill an animal by destroying the blood vessels in its brain? That’s what the “bird flu” does to cats. It turns the brain to mush.

Why? Because it has a polybasic cleavage site. What does that mean in simple English? A protein is made of amino acids. There are 22 of those found in the genetic code of life. Three of those, Arginine, Lysine and Histidine are basic amino acids, the opposite of acidic.

When you put a whole bunch of those basic amino acids close together in a protein, you get a polybasic site. This allows enzymes our cells produce to attach there. Those enzymes can then cut up the protein at that particular site.

The effect this has, is that when a protein of a virus develops such a polybasic site in the exact right spot, it can start to infect different cell types, cell types that produce these particular enzymes, that would normally not be available for such a virus to infect. One of those enzymes is furin, but there are others too. That’s why you hear this term “polybasic furin cleavage site” thrown around a lot, about SARS-COV-2.

But the influenza virus, that we know for causing “the flu”, normally has no polybasic cleavage site. It only has been found to develop the polybasic cleavage site, under two conditions:

-Cell cultures in a lab.

-Massive factory farms full of birds

And we know why this is. With at least five of these basic amino acids in a row, you call the cleavage site “polybasic”. When you see three or four of these basic amino acids in a row, you call the cleavage site “multibasic”. Normal influenza, the type that infects us humans and other animals, has just one basic amino acid, that only allows enzymes found in our lungs to cleave it. We call this “monobasic”.

And the problem is as following: To get to the polybasic cleavage site variety as a virus, you first have to evolve the multibasic variety, out of the monobasic variety. But the multibasic variety, is just not very good at functioning as a virus. It’s bad at competing in the wild.

On the other hand, when such a virus emerges in a factory farm, where it faces no competition from other viruses, no pre-existing immunity against influenza and birds with poor health, it can easily spread there, mutate to add more basic amino acids and evolve into the polybasic cleavage site variety. And unlike the intermediary step, the multibasic variety, the polybasic variety does manage to survive in the wild, so now wild birds can start spreading it from one chicken broiler to another.

I’ll quote the study for you:
Low pathogenicity avian influenza viruses (LPAIVs) are generally asymptomatic in their natural avian hosts. LPAIVs can evolve into highly pathogenic forms, which can affect avian and human populations with devastating consequences. The switch to highly pathogenic avian influenza virus (HPAIV) from LPAIV precursors requires the acquisition of multiple basic amino acids in the haemagglutinin cleavage site (HACS) motif. Through reverse genetics of an H5N1 HPAIV, and experimental infection of chickens, we determined that viruses containing five or more basic amino acids in the HACS motif were preferentially selected over those with three to four basic amino acids, leading to rapid replacement with virus types containing extended HACS motifs. Conversely, viruses harbouring low pathogenicity motifs containing two basic amino acids did not readily evolve to extended forms, suggesting that a single insertion of a basic amino acid into the cleavage site motif of low-pathogenic viruses may lead to escalating selection for extended motifs. Our results may explain why mid-length forms are rarely detected in nature. The stability of the short motif suggests that pathogenicity switching may require specific conditions of intense selection pressure (such as with high host density) to boost selection of the initial mid-length HACS forms.
That last sentence I made bold, because this is the important thing to understand: These viruses are NOT natural! They’re a product of humans putting birds in these conditions:

1broiler-1024x554.jpg


When you put the birds in HELL, you give birth to a virus from HELL.

This thing was born in the 90’s in China. They tried vaccinating against it, but it didn’t work, it just accelerated its evolution and encouraged it to spill over into other animals.

The important thing to understand is as following: It’s the polybasic cleavage site, that allows influenza viruses to infect endothelial cells, in humans as well as in birds. Remove the polybasic cleavage site and it becomes like normal influenza, in that it can’t replicate in the endothelial cells anymore. I quote:

To test the permissiveness of pulmonary endothelial cells to virus infection, we compared the replication of selected seasonal, pandemic (2009 H1N1 and 1918), and potentially pandemic (H5N1) influenza virus strains. We observed that these cells support productive replication only of HPAI H5N1 viruses, which preferentially enter through and are released from the apical surface of polarized human endothelial monolayers. Furthermore, A/Thailand/16/2004 and A/Vietnam/1203/2004 (VN/1203) H5N1 viruses, which exhibit heightened virulence in mammalian models, replicated to higher titers than less virulent H5N1 strains. VN/1203 infection caused a significant decrease in endothelial cell proliferation compared to other subtype viruses. VN/1203 virus was also found to be a potent inducer of cytokines and adhesion molecules known to regulate inflammation during acute lung injury. Deletion of the H5 hemagglutinin (HA) multibasic cleavage site did not affect virus infectivity but resulted in decreased virus replication in endothelial cells.

The endothelial cells, are the cells that line all your blood vessels, including in your brain.

Different cell types, will have different machinery operating inside of them. When the virus develops the polybasic cleavage site that allows it to switch to the endothelial cells, that means it has to figure out how to make optimal use of those cells, rather than the cells in the lungs it would normally rely on.

So what happens next is that the internal genes start to change too, to enable efficient use of the new cell types it can infect. The polybasic cleavage site makes the virus deadlier, but it’s not enough on its own to get the results we now see in the chickens, where 90% of them die within 48 hours of infection. All sorts of other changes start to happen, once the virus has the polybasic cleavage site.

This is why it’s insanity, to expect that once the bird flu becomes a virus that jumps between humans, it will eventually evolve to become like the normal flu we’re used to.

Do you expect whales to crawl back on land again at some point? Do you expect bats to lose their wings one day and live like mice? When such a sudden dramatic shift happens in the cell types this virus uses to survive in, it becomes forced to adapt to those conditions. It can’t just lose the polybasic cleavage site and go back to being a normal influenza virus, because then without the polybasic cleavage site, it still has those other mutations. So then it’s just a poor influenza virus, unable to compete with other influenza viruses.

Some of those other mutations involve big deletions of twenty amino acids in a row. You don’t just reverse a mutation like that, that’s incredibly hard for natural selection to do.

Once this virus goes human-to-human, people imagine it will be like the 1918 influenza pandemic. First a whole bunch of people die, but then it mutates and starts behaving like a normal flu virus. That’s not going to happen.

To start with, we never see it grow milder when it’s given to animals. In such animal passage studies, it grows deadlier with every jump it makes. That’s what you’re seeing with the cows right now too, it was pretty mild in Texas when we first discovered it in cows, but now in California it’s killing huge numbers of them.

But second, it’s always going to behave like a fundamentally different virus from the influenza we know.

The 1918 H1N1 virus, did NOT have a polybasic cleavage site. The 1918 virus, can NOT infect endothelial cells. So it can’t offer you lessons for what’s going to happen now. The polybasic cleavage site, is a consequence of our factory farms. Those factory farms, are a new thing:

1poultry.jpg


So we have never seen anything like this virus in our population before, because we never before created the conditions in which a virus like this can come into existence.

It’s not going to behave like any influenza viruses that we are used to.

And it’s not just going to return to behaving like a normal influenza virus after a few waves through our population.

I will readily admit, that I love a good horror story. But modern animal agriculture, is much better at creating horror stories, than I can ever hope to be.

This is the reality of what we’re dealing with.

When you hear about bird flu on the news, those people should be reminding you of these four points:
  1. It does not behave like a normal flu virus.
  2. It’s not natural, it could only come into existence in our giant chicken broilers.
  3. It’s not just going to turn into a normal flu again eventually.
  4. It damages the blood vessels in your brain.
Those are the facts. When they are not telling you those four points, then they’re just training you to say “it’s all bullshit”. You will say: “Oh the flu? I’ve had the flu before.”

I honestly really don’t care how many people it kills, it’s going to be a horror show either way. Your endothelial cells lining your blood vessels, are basically part of your immune system. Unlike most cells, they are able to produce huge amounts of Interferon alpha, a molecule basically designed by evolution to interfere in every step of a viral reproduction cycle.

That’s what we see in this virus, it causes the infected cells to produce huge amounts of it.

So you end up with this virus in the blood vessels in your brain. They produce huge amounts of Interferon Alpha. You can reliably induce depression in a person, by injecting them with interferon alpha, which is sometimes done to treat a viral infection. They suffer severe depression for weeks afterwards, often it recurs later on.

Even if you survive it, it’s a virus that’s going to screw with your mind, by putting your immune system in your brain on high alert, kind of similar to SARS-COV-2.

What we see in cows right now, is that it damages the immune system, they tend to succumb not to the direct effects of the virus itself, but to subsequent bacterial infections. Again, it’s not a normal flu virus. It is found to replicate much better in myeloid cells than normal influenza. What are those? Blood cells derived from bone marrow. It includes neutrophils, macrophages and other cells of your innate immune system.

They’re going to try to vaccinate against it, which will go about as well as you would expect. We have at least three separate strains now in the United States, including one jumping from chickens into humans and one jumping from cattle into humans.

The virus evolved in chickens who were being actively vaccinated against it. It’s inherently vaccine-resistant and humans already have adaptive immunity against it from exposure to regular influenza. So the vaccines are not going to do much against it. Vaccination just selects for neurovirulence, as the antibodies normally don’t pass the blood brain-barrier.

My hope is that at least some of the population will have protection from the natural killer cells and monocytes that migrate into the brain when you are infected by SARS-COV-2 without having been vaccinated. They don’t migrate into the brain when you’re infected while vaccinated, in which case your body just deploys antibodies that are not going to be neutralizing for influenza. The endothelial cells themselves should also have been trained by now.

It’s not looking good. But people just entirely don’t care, I’m accused of fear-mongering. The reality is: Twenty percent of your cows in California are dying from this. It killed 96% out of 17,000 of the elephant seal pups in South America.

It’s already causing ecological disasters around the world. But people don’t want to see it, the right wingers want to think Bill Gates and Klaus Schwab invented this to force them to eat bugs. But that’s honestly not half as stupid, as the “I believe in science” types, who think we’re going to solve this by vaccinating anything that moves.

We tried that in the 90’s, when it first showed up in our poultry. It didn’t work. It made it worse, by increasing the genetic diversity of these viruses, thereby allowing them to jump into more animal species. That’s why we are where we are now.

Sorry, but this is the story that’s going to dominate the remainder of your life. Resource depletion and climate change are big problems, but they ramp up slowly. This one, this one ramps up fast.

How do you expect to run a farm and produce milk, when half your cows die in a single month? That’s the reality some farmers in California now face.

Something like this just bankrupts farmers. And at first the government may try to prop up the farmers to keep business as usual going. But eventually you realize that it just no longer works. You can just no longer produce milk at an affordable price and your workers are bleeding from their eyeballs. That’s when entire villages in places like South Dakota, where milk is the only thing being produced, just become non-viable. Anyone who is not directly involved in producing milk there, is indirectly dependent on it.

We closed our eyes for a tragedy that happens on a constant basis:

2 min 26 sec
View: https://www.youtube.com/watch?v=HXJrk5vF4R8

So now we’ll face one of our own.

.
 

naegling62

Veteran Member
Radagast just did a piece on bird flu today, I'll add it to go with that tweet. Keep in mind though he is a very strong proponent of vegetarianism which is evident in this piece.



(fair use applies)

What nobody wants to hear about bird flu
Radagast
November 3, 2024

Look, this is my blog, so I get to decide what I want to write about. I don’t have a bunch of fat American MAGA boomers sending me 5 dollars a month in exchange for telling them that Joe Biden’s climate change hysteria is going to make our meat and eggs expensive.

I look at this website a bit like my legacy. I will die one day and then I’ll be able to take comfort in the fact that I sought to tell people the truth, instead of the popular lie that makes you money. I don’t have to administer you addictive brain-opioids, that lull you to sleep. I get to tell you what you don’t want to hear. I get to tell you, the truth. People don’t lie to you to deceive you. They lie to you because you prefer being lied to.

But this is the truth and you’re not going to like it. The bird flu, is not “flu”. Yes, it’s technically an influenza virus, in the same sense as a bat is technically a mammal. But when you think of a mammal, you think of an animal that lives on land, not an animal that flies in the sky.

How many influenza viruses can you think of, that kill an animal by destroying the blood vessels in its brain? That’s what the “bird flu” does to cats. It turns the brain to mush.

Why? Because it has a polybasic cleavage site. What does that mean in simple English? A protein is made of amino acids. There are 22 of those found in the genetic code of life. Three of those, Arginine, Lysine and Histidine are basic amino acids, the opposite of acidic.

When you put a whole bunch of those basic amino acids close together in a protein, you get a polybasic site. This allows enzymes our cells produce to attach there. Those enzymes can then cut up the protein at that particular site.

The effect this has, is that when a protein of a virus develops such a polybasic site in the exact right spot, it can start to infect different cell types, cell types that produce these particular enzymes, that would normally not be available for such a virus to infect. One of those enzymes is furin, but there are others too. That’s why you hear this term “polybasic furin cleavage site” thrown around a lot, about SARS-COV-2.

But the influenza virus, that we know for causing “the flu”, normally has no polybasic cleavage site. It only has been found to develop the polybasic cleavage site, under two conditions:

-Cell cultures in a lab.

-Massive factory farms full of birds

And we know why this is. With at least five of these basic amino acids in a row, you call the cleavage site “polybasic”. When you see three or four of these basic amino acids in a row, you call the cleavage site “multibasic”. Normal influenza, the type that infects us humans and other animals, has just one basic amino acid, that only allows enzymes found in our lungs to cleave it. We call this “monobasic”.

And the problem is as following: To get to the polybasic cleavage site variety as a virus, you first have to evolve the multibasic variety, out of the monobasic variety. But the multibasic variety, is just not very good at functioning as a virus. It’s bad at competing in the wild.

On the other hand, when such a virus emerges in a factory farm, where it faces no competition from other viruses, no pre-existing immunity against influenza and birds with poor health, it can easily spread there, mutate to add more basic amino acids and evolve into the polybasic cleavage site variety. And unlike the intermediary step, the multibasic variety, the polybasic variety does manage to survive in the wild, so now wild birds can start spreading it from one chicken broiler to another.

I’ll quote the study for you:
Low pathogenicity avian influenza viruses (LPAIVs) are generally asymptomatic in their natural avian hosts. LPAIVs can evolve into highly pathogenic forms, which can affect avian and human populations with devastating consequences. The switch to highly pathogenic avian influenza virus (HPAIV) from LPAIV precursors requires the acquisition of multiple basic amino acids in the haemagglutinin cleavage site (HACS) motif. Through reverse genetics of an H5N1 HPAIV, and experimental infection of chickens, we determined that viruses containing five or more basic amino acids in the HACS motif were preferentially selected over those with three to four basic amino acids, leading to rapid replacement with virus types containing extended HACS motifs. Conversely, viruses harbouring low pathogenicity motifs containing two basic amino acids did not readily evolve to extended forms, suggesting that a single insertion of a basic amino acid into the cleavage site motif of low-pathogenic viruses may lead to escalating selection for extended motifs. Our results may explain why mid-length forms are rarely detected in nature. The stability of the short motif suggests that pathogenicity switching may require specific conditions of intense selection pressure (such as with high host density) to boost selection of the initial mid-length HACS forms.
That last sentence I made bold, because this is the important thing to understand: These viruses are NOT natural! They’re a product of humans putting birds in these conditions:

1broiler-1024x554.jpg


When you put the birds in HELL, you give birth to a virus from HELL.

This thing was born in the 90’s in China. They tried vaccinating against it, but it didn’t work, it just accelerated its evolution and encouraged it to spill over into other animals.

The important thing to understand is as following: It’s the polybasic cleavage site, that allows influenza viruses to infect endothelial cells, in humans as well as in birds. Remove the polybasic cleavage site and it becomes like normal influenza, in that it can’t replicate in the endothelial cells anymore. I quote:

To test the permissiveness of pulmonary endothelial cells to virus infection, we compared the replication of selected seasonal, pandemic (2009 H1N1 and 1918), and potentially pandemic (H5N1) influenza virus strains. We observed that these cells support productive replication only of HPAI H5N1 viruses, which preferentially enter through and are released from the apical surface of polarized human endothelial monolayers. Furthermore, A/Thailand/16/2004 and A/Vietnam/1203/2004 (VN/1203) H5N1 viruses, which exhibit heightened virulence in mammalian models, replicated to higher titers than less virulent H5N1 strains. VN/1203 infection caused a significant decrease in endothelial cell proliferation compared to other subtype viruses. VN/1203 virus was also found to be a potent inducer of cytokines and adhesion molecules known to regulate inflammation during acute lung injury. Deletion of the H5 hemagglutinin (HA) multibasic cleavage site did not affect virus infectivity but resulted in decreased virus replication in endothelial cells.

The endothelial cells, are the cells that line all your blood vessels, including in your brain.

Different cell types, will have different machinery operating inside of them. When the virus develops the polybasic cleavage site that allows it to switch to the endothelial cells, that means it has to figure out how to make optimal use of those cells, rather than the cells in the lungs it would normally rely on.

So what happens next is that the internal genes start to change too, to enable efficient use of the new cell types it can infect. The polybasic cleavage site makes the virus deadlier, but it’s not enough on its own to get the results we now see in the chickens, where 90% of them die within 48 hours of infection. All sorts of other changes start to happen, once the virus has the polybasic cleavage site.

This is why it’s insanity, to expect that once the bird flu becomes a virus that jumps between humans, it will eventually evolve to become like the normal flu we’re used to.

Do you expect whales to crawl back on land again at some point? Do you expect bats to lose their wings one day and live like mice? When such a sudden dramatic shift happens in the cell types this virus uses to survive in, it becomes forced to adapt to those conditions. It can’t just lose the polybasic cleavage site and go back to being a normal influenza virus, because then without the polybasic cleavage site, it still has those other mutations. So then it’s just a poor influenza virus, unable to compete with other influenza viruses.

Some of those other mutations involve big deletions of twenty amino acids in a row. You don’t just reverse a mutation like that, that’s incredibly hard for natural selection to do.

Once this virus goes human-to-human, people imagine it will be like the 1918 influenza pandemic. First a whole bunch of people die, but then it mutates and starts behaving like a normal flu virus. That’s not going to happen.

To start with, we never see it grow milder when it’s given to animals. In such animal passage studies, it grows deadlier with every jump it makes. That’s what you’re seeing with the cows right now too, it was pretty mild in Texas when we first discovered it in cows, but now in California it’s killing huge numbers of them.

But second, it’s always going to behave like a fundamentally different virus from the influenza we know.

The 1918 H1N1 virus, did NOT have a polybasic cleavage site. The 1918 virus, can NOT infect endothelial cells. So it can’t offer you lessons for what’s going to happen now. The polybasic cleavage site, is a consequence of our factory farms. Those factory farms, are a new thing:

1poultry.jpg


So we have never seen anything like this virus in our population before, because we never before created the conditions in which a virus like this can come into existence.

It’s not going to behave like any influenza viruses that we are used to.

And it’s not just going to return to behaving like a normal influenza virus after a few waves through our population.

I will readily admit, that I love a good horror story. But modern animal agriculture, is much better at creating horror stories, than I can ever hope to be.

This is the reality of what we’re dealing with.

When you hear about bird flu on the news, those people should be reminding you of these four points:
  1. It does not behave like a normal flu virus.
  2. It’s not natural, it could only come into existence in our giant chicken broilers.
  3. It’s not just going to turn into a normal flu again eventually.
  4. It damages the blood vessels in your brain.
Those are the facts. When they are not telling you those four points, then they’re just training you to say “it’s all bullshit”. You will say: “Oh the flu? I’ve had the flu before.”

I honestly really don’t care how many people it kills, it’s going to be a horror show either way. Your endothelial cells lining your blood vessels, are basically part of your immune system. Unlike most cells, they are able to produce huge amounts of Interferon alpha, a molecule basically designed by evolution to interfere in every step of a viral reproduction cycle.

That’s what we see in this virus, it causes the infected cells to produce huge amounts of it.

So you end up with this virus in the blood vessels in your brain. They produce huge amounts of Interferon Alpha. You can reliably induce depression in a person, by injecting them with interferon alpha, which is sometimes done to treat a viral infection. They suffer severe depression for weeks afterwards, often it recurs later on.

Even if you survive it, it’s a virus that’s going to screw with your mind, by putting your immune system in your brain on high alert, kind of similar to SARS-COV-2.

What we see in cows right now, is that it damages the immune system, they tend to succumb not to the direct effects of the virus itself, but to subsequent bacterial infections. Again, it’s not a normal flu virus. It is found to replicate much better in myeloid cells than normal influenza. What are those? Blood cells derived from bone marrow. It includes neutrophils, macrophages and other cells of your innate immune system.

They’re going to try to vaccinate against it, which will go about as well as you would expect. We have at least three separate strains now in the United States, including one jumping from chickens into humans and one jumping from cattle into humans.

The virus evolved in chickens who were being actively vaccinated against it. It’s inherently vaccine-resistant and humans already have adaptive immunity against it from exposure to regular influenza. So the vaccines are not going to do much against it. Vaccination just selects for neurovirulence, as the antibodies normally don’t pass the blood brain-barrier.

My hope is that at least some of the population will have protection from the natural killer cells and monocytes that migrate into the brain when you are infected by SARS-COV-2 without having been vaccinated. They don’t migrate into the brain when you’re infected while vaccinated, in which case your body just deploys antibodies that are not going to be neutralizing for influenza. The endothelial cells themselves should also have been trained by now.

It’s not looking good. But people just entirely don’t care, I’m accused of fear-mongering. The reality is: Twenty percent of your cows in California are dying from this. It killed 96% out of 17,000 of the elephant seal pups in South America.

It’s already causing ecological disasters around the world. But people don’t want to see it, the right wingers want to think Bill Gates and Klaus Schwab invented this to force them to eat bugs. But that’s honestly not half as stupid, as the “I believe in science” types, who think we’re going to solve this by vaccinating anything that moves.

We tried that in the 90’s, when it first showed up in our poultry. It didn’t work. It made it worse, by increasing the genetic diversity of these viruses, thereby allowing them to jump into more animal species. That’s why we are where we are now.

Sorry, but this is the story that’s going to dominate the remainder of your life. Resource depletion and climate change are big problems, but they ramp up slowly. This one, this one ramps up fast.

How do you expect to run a farm and produce milk, when half your cows die in a single month? That’s the reality some farmers in California now face.

Something like this just bankrupts farmers. And at first the government may try to prop up the farmers to keep business as usual going. But eventually you realize that it just no longer works. You can just no longer produce milk at an affordable price and your workers are bleeding from their eyeballs. That’s when entire villages in places like South Dakota, where milk is the only thing being produced, just become non-viable. Anyone who is not directly involved in producing milk there, is indirectly dependent on it.

We closed our eyes for a tragedy that happens on a constant basis:

2 min 26 sec
View: https://www.youtube.com/watch?v=HXJrk5vF4R8

So now we’ll face one of our own.

.
Great article and explanation. Politics was not necessary to be included by him. BTW, some of the healthiest fit individuals I know are MAGA.
 

Zoner

Veteran Member
Radagast just did a piece on bird flu today, I'll add it to go with that tweet. Keep in mind though he is a very strong proponent of vegetarianism which is evident in this piece.



(fair use applies)

What nobody wants to hear about bird flu
Radagast
November 3, 2024

Look, this is my blog, so I get to decide what I want to write about. I don’t have a bunch of fat American MAGA boomers sending me 5 dollars a month in exchange for telling them that Joe Biden’s climate change hysteria is going to make our meat and eggs expensive.

I look at this website a bit like my legacy. I will die one day and then I’ll be able to take comfort in the fact that I sought to tell people the truth, instead of the popular lie that makes you money. I don’t have to administer you addictive brain-opioids, that lull you to sleep. I get to tell you what you don’t want to hear. I get to tell you, the truth. People don’t lie to you to deceive you. They lie to you because you prefer being lied to.

But this is the truth and you’re not going to like it. The bird flu, is not “flu”. Yes, it’s technically an influenza virus, in the same sense as a bat is technically a mammal. But when you think of a mammal, you think of an animal that lives on land, not an animal that flies in the sky.

How many influenza viruses can you think of, that kill an animal by destroying the blood vessels in its brain? That’s what the “bird flu” does to cats. It turns the brain to mush.

Why? Because it has a polybasic cleavage site. What does that mean in simple English? A protein is made of amino acids. There are 22 of those found in the genetic code of life. Three of those, Arginine, Lysine and Histidine are basic amino acids, the opposite of acidic.

When you put a whole bunch of those basic amino acids close together in a protein, you get a polybasic site. This allows enzymes our cells produce to attach there. Those enzymes can then cut up the protein at that particular site.

The effect this has, is that when a protein of a virus develops such a polybasic site in the exact right spot, it can start to infect different cell types, cell types that produce these particular enzymes, that would normally not be available for such a virus to infect. One of those enzymes is furin, but there are others too. That’s why you hear this term “polybasic furin cleavage site” thrown around a lot, about SARS-COV-2.

But the influenza virus, that we know for causing “the flu”, normally has no polybasic cleavage site. It only has been found to develop the polybasic cleavage site, under two conditions:

-Cell cultures in a lab.

-Massive factory farms full of birds

And we know why this is. With at least five of these basic amino acids in a row, you call the cleavage site “polybasic”. When you see three or four of these basic amino acids in a row, you call the cleavage site “multibasic”. Normal influenza, the type that infects us humans and other animals, has just one basic amino acid, that only allows enzymes found in our lungs to cleave it. We call this “monobasic”.

And the problem is as following: To get to the polybasic cleavage site variety as a virus, you first have to evolve the multibasic variety, out of the monobasic variety. But the multibasic variety, is just not very good at functioning as a virus. It’s bad at competing in the wild.

On the other hand, when such a virus emerges in a factory farm, where it faces no competition from other viruses, no pre-existing immunity against influenza and birds with poor health, it can easily spread there, mutate to add more basic amino acids and evolve into the polybasic cleavage site variety. And unlike the intermediary step, the multibasic variety, the polybasic variety does manage to survive in the wild, so now wild birds can start spreading it from one chicken broiler to another.

I’ll quote the study for you:
Low pathogenicity avian influenza viruses (LPAIVs) are generally asymptomatic in their natural avian hosts. LPAIVs can evolve into highly pathogenic forms, which can affect avian and human populations with devastating consequences. The switch to highly pathogenic avian influenza virus (HPAIV) from LPAIV precursors requires the acquisition of multiple basic amino acids in the haemagglutinin cleavage site (HACS) motif. Through reverse genetics of an H5N1 HPAIV, and experimental infection of chickens, we determined that viruses containing five or more basic amino acids in the HACS motif were preferentially selected over those with three to four basic amino acids, leading to rapid replacement with virus types containing extended HACS motifs. Conversely, viruses harbouring low pathogenicity motifs containing two basic amino acids did not readily evolve to extended forms, suggesting that a single insertion of a basic amino acid into the cleavage site motif of low-pathogenic viruses may lead to escalating selection for extended motifs. Our results may explain why mid-length forms are rarely detected in nature. The stability of the short motif suggests that pathogenicity switching may require specific conditions of intense selection pressure (such as with high host density) to boost selection of the initial mid-length HACS forms.
That last sentence I made bold, because this is the important thing to understand: These viruses are NOT natural! They’re a product of humans putting birds in these conditions:

1broiler-1024x554.jpg


When you put the birds in HELL, you give birth to a virus from HELL.

This thing was born in the 90’s in China. They tried vaccinating against it, but it didn’t work, it just accelerated its evolution and encouraged it to spill over into other animals.

The important thing to understand is as following: It’s the polybasic cleavage site, that allows influenza viruses to infect endothelial cells, in humans as well as in birds. Remove the polybasic cleavage site and it becomes like normal influenza, in that it can’t replicate in the endothelial cells anymore. I quote:

To test the permissiveness of pulmonary endothelial cells to virus infection, we compared the replication of selected seasonal, pandemic (2009 H1N1 and 1918), and potentially pandemic (H5N1) influenza virus strains. We observed that these cells support productive replication only of HPAI H5N1 viruses, which preferentially enter through and are released from the apical surface of polarized human endothelial monolayers. Furthermore, A/Thailand/16/2004 and A/Vietnam/1203/2004 (VN/1203) H5N1 viruses, which exhibit heightened virulence in mammalian models, replicated to higher titers than less virulent H5N1 strains. VN/1203 infection caused a significant decrease in endothelial cell proliferation compared to other subtype viruses. VN/1203 virus was also found to be a potent inducer of cytokines and adhesion molecules known to regulate inflammation during acute lung injury. Deletion of the H5 hemagglutinin (HA) multibasic cleavage site did not affect virus infectivity but resulted in decreased virus replication in endothelial cells.

The endothelial cells, are the cells that line all your blood vessels, including in your brain.

Different cell types, will have different machinery operating inside of them. When the virus develops the polybasic cleavage site that allows it to switch to the endothelial cells, that means it has to figure out how to make optimal use of those cells, rather than the cells in the lungs it would normally rely on.

So what happens next is that the internal genes start to change too, to enable efficient use of the new cell types it can infect. The polybasic cleavage site makes the virus deadlier, but it’s not enough on its own to get the results we now see in the chickens, where 90% of them die within 48 hours of infection. All sorts of other changes start to happen, once the virus has the polybasic cleavage site.

This is why it’s insanity, to expect that once the bird flu becomes a virus that jumps between humans, it will eventually evolve to become like the normal flu we’re used to.

Do you expect whales to crawl back on land again at some point? Do you expect bats to lose their wings one day and live like mice? When such a sudden dramatic shift happens in the cell types this virus uses to survive in, it becomes forced to adapt to those conditions. It can’t just lose the polybasic cleavage site and go back to being a normal influenza virus, because then without the polybasic cleavage site, it still has those other mutations. So then it’s just a poor influenza virus, unable to compete with other influenza viruses.

Some of those other mutations involve big deletions of twenty amino acids in a row. You don’t just reverse a mutation like that, that’s incredibly hard for natural selection to do.

Once this virus goes human-to-human, people imagine it will be like the 1918 influenza pandemic. First a whole bunch of people die, but then it mutates and starts behaving like a normal flu virus. That’s not going to happen.

To start with, we never see it grow milder when it’s given to animals. In such animal passage studies, it grows deadlier with every jump it makes. That’s what you’re seeing with the cows right now too, it was pretty mild in Texas when we first discovered it in cows, but now in California it’s killing huge numbers of them.

But second, it’s always going to behave like a fundamentally different virus from the influenza we know.

The 1918 H1N1 virus, did NOT have a polybasic cleavage site. The 1918 virus, can NOT infect endothelial cells. So it can’t offer you lessons for what’s going to happen now. The polybasic cleavage site, is a consequence of our factory farms. Those factory farms, are a new thing:

1poultry.jpg


So we have never seen anything like this virus in our population before, because we never before created the conditions in which a virus like this can come into existence.

It’s not going to behave like any influenza viruses that we are used to.

And it’s not just going to return to behaving like a normal influenza virus after a few waves through our population.

I will readily admit, that I love a good horror story. But modern animal agriculture, is much better at creating horror stories, than I can ever hope to be.

This is the reality of what we’re dealing with.

When you hear about bird flu on the news, those people should be reminding you of these four points:
  1. It does not behave like a normal flu virus.
  2. It’s not natural, it could only come into existence in our giant chicken broilers.
  3. It’s not just going to turn into a normal flu again eventually.
  4. It damages the blood vessels in your brain.
Those are the facts. When they are not telling you those four points, then they’re just training you to say “it’s all bullshit”. You will say: “Oh the flu? I’ve had the flu before.”

I honestly really don’t care how many people it kills, it’s going to be a horror show either way. Your endothelial cells lining your blood vessels, are basically part of your immune system. Unlike most cells, they are able to produce huge amounts of Interferon alpha, a molecule basically designed by evolution to interfere in every step of a viral reproduction cycle.

That’s what we see in this virus, it causes the infected cells to produce huge amounts of it.

So you end up with this virus in the blood vessels in your brain. They produce huge amounts of Interferon Alpha. You can reliably induce depression in a person, by injecting them with interferon alpha, which is sometimes done to treat a viral infection. They suffer severe depression for weeks afterwards, often it recurs later on.

Even if you survive it, it’s a virus that’s going to screw with your mind, by putting your immune system in your brain on high alert, kind of similar to SARS-COV-2.

What we see in cows right now, is that it damages the immune system, they tend to succumb not to the direct effects of the virus itself, but to subsequent bacterial infections. Again, it’s not a normal flu virus. It is found to replicate much better in myeloid cells than normal influenza. What are those? Blood cells derived from bone marrow. It includes neutrophils, macrophages and other cells of your innate immune system.

They’re going to try to vaccinate against it, which will go about as well as you would expect. We have at least three separate strains now in the United States, including one jumping from chickens into humans and one jumping from cattle into humans.

The virus evolved in chickens who were being actively vaccinated against it. It’s inherently vaccine-resistant and humans already have adaptive immunity against it from exposure to regular influenza. So the vaccines are not going to do much against it. Vaccination just selects for neurovirulence, as the antibodies normally don’t pass the blood brain-barrier.

My hope is that at least some of the population will have protection from the natural killer cells and monocytes that migrate into the brain when you are infected by SARS-COV-2 without having been vaccinated. They don’t migrate into the brain when you’re infected while vaccinated, in which case your body just deploys antibodies that are not going to be neutralizing for influenza. The endothelial cells themselves should also have been trained by now.

It’s not looking good. But people just entirely don’t care, I’m accused of fear-mongering. The reality is: Twenty percent of your cows in California are dying from this. It killed 96% out of 17,000 of the elephant seal pups in South America.

It’s already causing ecological disasters around the world. But people don’t want to see it, the right wingers want to think Bill Gates and Klaus Schwab invented this to force them to eat bugs. But that’s honestly not half as stupid, as the “I believe in science” types, who think we’re going to solve this by vaccinating anything that moves.

We tried that in the 90’s, when it first showed up in our poultry. It didn’t work. It made it worse, by increasing the genetic diversity of these viruses, thereby allowing them to jump into more animal species. That’s why we are where we are now.

Sorry, but this is the story that’s going to dominate the remainder of your life. Resource depletion and climate change are big problems, but they ramp up slowly. This one, this one ramps up fast.

How do you expect to run a farm and produce milk, when half your cows die in a single month? That’s the reality some farmers in California now face.

Something like this just bankrupts farmers. And at first the government may try to prop up the farmers to keep business as usual going. But eventually you realize that it just no longer works. You can just no longer produce milk at an affordable price and your workers are bleeding from their eyeballs. That’s when entire villages in places like South Dakota, where milk is the only thing being produced, just become non-viable. Anyone who is not directly involved in producing milk there, is indirectly dependent on it.

We closed our eyes for a tragedy that happens on a constant basis:

2 min 26 sec
View: https://www.youtube.com/watch?v=HXJrk5vF4R8

So now we’ll face one of our own.

.
Either God puts a stop to it or the world will come to an end as we know it.
A very scary piece. There’s not much to say except maybe thanks
 

Heliobas Disciple

TB Fanatic
Great article and explanation. Politics was not necessary to be included by him. BTW, some of the healthiest fit individuals I know are MAGA.

He has some strange beliefs and he's pretty stubborn about them. I try to just skip over the parts that aren't the pure science. I sometimes wonder to myself how I trust the science from someone who I disagree with on so much else he posts. But his science seems to make sense. Maybe because he's preaching to the choir on that for me. Or because he agrees with Geert on a lot of it. :shr:

HD
 

Heliobas Disciple

TB Fanatic
(fair use applies)


A Q&A with the FDA’s top vaccine regulator amid a fresh wave of disinformation
When it comes to safety debates, Peter Marks believes transparency is crucial

By Helen Branswell
Nov. 4, 2024

Vaccination policy in the United States could be in line for some fundamental changes, if Donald Trump is reelected and delivers on promises that long-time vaccine skeptic Robert Kennedy Jr. said the former president has made — including giving Kennedy authority over the country’s health agencies in a second Trump administration.

Even if none of that comes to pass, vaccine fatigue and disinformation abound in the wake of the Covid-19 pandemic. Public health authorities promoting vaccine use do so in an ever more challenging climate.

At a public forum last week, Peter Marks, the top vaccine regulator for the Food and Drug Administration, said the way to counter the movement is by being transparent.

“We have to be steadfast in this. Answer questions, be honest, that will ultimately take the day over the misinformation and disinformation, which is being done for non-health purposes,” he said during a panel discussion on fall vaccinations organized by the group Champions for Vaccine Education, Equity and Progress.

STAT reached out to Marks, the director of the FDA’s Center for Biologics Evaluation and Research, to talk about how vaccines are regulated in this country. He agreed, though the FDA stated in advance that he would not comment on individuals involved in the current political debate or anything they have said.

The following transcript of the conversation has been lightly edited for length and clarity.

Broadly speaking, we’re seeing a lot of vaccine skepticism lately. It’s in the news often. There’s a lot of misinformation out there. I don’t know, though, that we actually are seeing a huge drop in vaccination rates. I know there’s been some decline. Certainly for some vaccines, like the Covid vaccines, there’s been a drop-off. Is there more noise than actual reality around this topic?

I think we don’t know the full extent of the adverse effect on vaccination. We won’t know that until we see pockets of kids who haven’t gotten certain vaccines coming down with infectious diseases.

The problem is that it doesn’t take vaccination rates to drop off that much to start getting into problems here, where you lose herd immunity. So, I don’t disagree with you in the statement that it’s not like the sky is falling, but there are clearly pockets of people who have started to perhaps not take all of the appropriate vaccines. And there’s this kind of concept of ‘I’ll take the vaccines that I feel are important rather than the ones that are recommended.’ So I do think there’s some concern there that this could get worse. And we just don’t know the extent of the damage that’s been done to date.


Some of the skepticism appears to be rooted in claims that manufacturers don’t have to generate safety data before bringing a vaccine to market. Can you address that?

Vaccines are among the most well-monitored products. By definition, we cannot approve a vaccine unless the benefits greatly outweigh any risk.

The average vaccine, before it gets an approval in the United States, has been studied in something like 22,000 people treated with the vaccine. That’s the average. Some trials are smaller, some are more than that. The Covid vaccines had about 40,000 to 50,000 when they were ultimately approved, about 20,000 to 25,000 treated with a vaccine when they were [issued an emergency use authorization].

The bottom line is that there is a lot of safety data that we obtain before they go to market. And that’s in the clinical trial setting where there’s mandatory reporting of all adverse events, period. Not just serious adverse events but adverse events and serious adverse events. And then after licensure of these vaccines, there is reporting through the multiple overlapping safety systems.

We have the Vaccine Adverse Event Reporting System [VAERS], which seems to be very hard for people to understand. It’s basically a way for anyone [to report] any kind of adverse event, whether or not they know it to be related, after having a vaccine. So patients can report. Doctors can report. Other health care providers. Even companies.

And then we sort that out on the back end by getting additional data to figure out whether things truly are related or not. Now, part of the problem that we get into is that because that involves getting protected health information, the public doesn’t see what we see at the end of the day in terms of any potential relationship.


So, for instance, if somebody had a heart attack within a week of having a vaccination, VAERS will not show if that person has had a long history of cardiovascular problems?

That’s precisely correct. VAERS would not show the fact that they got the flu shot perhaps while they were hospitalized for unstable angina. And they had a heart attack while they were in the hospital. We sort it out on the back end.

The other safety systems are also very powerful, such as Sentinel Best, an active safety surveillance system. We have [data from] tens of millions of lives captured, either in health care-claims databases and/or electronic health records. We get data that’s obviously been de-identified. The confidentiality is maintained. But what we’re able to do is look at a population of individuals who have been vaccinated and a population who has not been vaccinated and see if certain adverse events — could be heart attacks, could be neurologic events such as Guillain-Barré syndrome [GBS], which we regularly look [for] with influenza vaccine, which we’ve looked for with respiratory syncytial virus vaccines. We constantly monitor that. And we actually make the data public. When we find things, we publish them or we post them on our websites.

Those who deny that the system is working just need to look at recent events. For instance, with the Janssen Covid vaccine, where we relatively rapidly within a few months of its deployment realized that it had a very serious adverse event — this thrombotic thrombocytopenia syndrome. It was identified. We warned providers. We relabeled the vaccine. And ultimately that vaccine, it’s not available anymore because Janssen decided that after all of the warnings on it, they would not proceed with a biologics license application and they withdrew the emergency use authorization.

So we do find things. Just like we often report a slight increase in risk of Guillain-Barré syndrome with the influenza vaccine. By the way, these are tough studies because there’s a background incidence of Guillain-Barré syndrome with flu infection too.


In fact, the rate of GBS is higher after flu infection than it is after flu vaccination, isn’t it?

Right!

I want to talk to you more about the post-licensure efforts, but first I want to ask you a little more about the pre-licensure activity. One of the things some critics of vaccines say is that they’re not tested in placebo-controlled double-blinded trials. If it’s a brand new vaccine for a new indication — like the new RSV vaccines — they were tested in double-blinded placebo-controlled trials.

The initial Covid vaccines were [tested in] double-blinded placebo-controlled trials.

The problem is that you get into these crazy criticisms where it’s almost like you can’t win for losing.


And in terms of a second-in-class vaccine — a new flu vaccine, for instance — or a next-generation vaccine improving on existing products, why is it that you can’t test them against placebo?

It’s very simple. When something becomes the standard of care, to deprive somebody of that standard of care is problematic. Instead you might test one vaccine against another, to see if [the new vaccine is] superior. That’s how the high-dose influenza vaccines were ultimately approved. It wasn’t against placebo, it was high-dose influenza vaccine against standard-dose influenza vaccine.


That reveals how you establish the efficacy of new vaccines for diseases where vaccines already exist on the market. What about safety? You don’t give those second-generation or competitor vaccines a pass on safety, do you? If you’re bringing a new flu shot to market, it also has to do all the safety testing, doesn’t it?

That’s exactly right. We basically have a requirement for a certain number of individuals to receive a vaccine and have safety data on it before we’ll approve that vaccine. The safety data set still has to be robust before we’ll give it an approval.

There is no skimping on safety in the vaccine world. We have very little risk tolerance when we give medicines or vaccines to healthy people. By definition, where we set the bar for vaccines is different from where we set them for other medical products because most people don’t want something bad to happen with them after they go get the flu vaccine. So we have to set the bar very high.


I think it’s also true that the bar is set higher still for vaccines for children. Covid vaccines weren’t approved for use in kids for about a year after they were for adults; you folks were criticized for this. There are people who would like the FDA to require manufacturers to test in pregnant people and in children at the same time as in adults. But there is this practice of effectively making sure something is safe in adults before going to kids. Is that correct?

That is generally the case. There are situations where we might have gone more rapidly into children. But with Covid-19, the magnitude of the problem in kids was not apparent until the Omicron wave. So the urgency was not there early in the pandemic. Had it been there, we might have moved a little faster, because the prospect of direct clinical benefit to children would have been clearer.

Remember, in early 2020 Covid-19 was viewed as a disease mainly of older people and adults. And the number of kids affected originally was pretty small. It wasn’t until Omicron that this became a real issue.


You were talking before about the follow-up work done after vaccines come to market and I think that what’s been happening with the RSV vaccines is a good example. There appeared to be a potential signal of GBS with a couple of the vaccines. And this is being followed closely. And in fact, the Advisory Committee on Immunization Practices, which advises the Centers for Disease Control and Prevention on how vaccines should be used, has been quite conservative in its recommendations for those vaccines. It wants answers about the risk of GBS before it recommends them more broadly.

That’s another example of the fact that people are watching very closely. And the focus on vaccine safety, I think it’s mirrored by the fact that you have not just one but two vaccine advisory committees. You have FDA’s advisory committee [the Vaccines and Related Biological Products Advisory Committee] that meets and discusses the risk-benefit profile of vaccines. And then you have the ACIP that looks at an even broader swath of data because they can look at real-world evidence and data that FDA doesn’t look at. And they once again are looking at safety data to see if they feel that, even for an FDA-approved vaccine, whether it should be deployed across the population that it might have been approved for.


You mentioned earlier that you almost can’t win for losing with some of these arguments. One of the things that I find interesting is that the agencies share information. So there’s been discussion publicly about the GBS risk with the RSV vaccines. On the one hand that might actually feed the anti-vaccine concerns, but if you didn’t, wouldn’t you be just roasted forever?

Being transparent about these issues is the right thing to do. And probably the most important thing to do is to try to continue to educate people that there are small risks with vaccines but those small risks are greatly outweighed by their potential benefits.

We have to make sure that people understand that with our vaccines, we don’t approve them unless we think that the number of deaths or the number of serious illnesses prevented [by them] greatly, greatly outweigh any adverse effects from the vaccines.


That’s a bit challenging, though, isn’t it? Because you’re talking about benefits across the population versus risk to the individual?

But the chance that an individual, for instance with a Covid-19 vaccine, [will experience] a serious adverse event is remarkably small. And the chance of benefit to the individual is not insignificant. And obviously the older you are, the greater the potential benefit with that particular infectious disease.

When you think about something like measles, measles is an infectious disease that kills children. You don’t need to be a rocket scientist for that one because outside of the United States, in Asia and Africa, there are still 90,000-plus kids that will die of measles encephalitis or pneumonitis in the next year because they just don’t have access to a measles vaccine. And before the advent of the measles vaccine, it was something like 2.5 or three kids per million in the United States died per year of measles. Now we have an effective vaccine.

Yes, there’s a rare — it’s like a one in 50,000, I think — risk of febrile seizures after measles vaccination. [The FDA later clarified that an estimated 3 in 10,000 children experience febrile seizures after measles vaccination, but there are no lasting effects.] And there’s an even smaller risk of blood clotting disorders. But at the end of the day, what you’re doing is preventing an infectious disease, which if it were to become widespread in the United States again, would likely cost one in 1,000 children their lives.

So that’s the kind of calculus you’re taking. An occasional adverse event, an occasional potentially serious [adverse event] at the rate of one in tens of thousands in order to save one in 1,000.

I think one thing we have learned about vaccination: If we’re honest about this, if we’re transparent, hopefully people will understand the benefits-risk [calculations] here and feel confident in their use, knowing that the risks are very small, the benefits are very much present.
 

Heliobas Disciple

TB Fanatic
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New study of seven million records reveals who gets long COVID in Australia
by Andrew Taylor, Macquarie University
November 4, 2024

A study of 7 million medical records found that in Australia, patients with long COVID are more likely to be women than men, or people aged 40–59 and those living in a high socioeconomic area. They usually have pre-existing health problems.

The findings, published by Macquarie University's Australian Institute of Health Innovation in the Medical Journal of Australia, add key insights about the demographics and clinical profile of people most likely to be diagnosed with long COVID.

The global COVID pandemic was declared over by health authorities in 2023, but the impact of long COVID continues to pose a challenge to medical care and research.

Most people infected with SARS-CoV-2 (COVID) fully recover after a few weeks, but some patients face persistent symptoms for many months after the infection.

There is no universally agreed definition of long COVID, but common symptoms include shortness of breath, cough, chest pain, fatigue, brain fog, dizziness, abdominal pain or nausea and even organ damage.

The Australian Institute of Health and Welfare estimates up to 10% of COVID patients will develop long COVID, imposing a significant burden on the health system and economy. But the true frequency and factors associated with long COVID in Australia is poorly understood, impeding evidence-based interventions to treat and provide services to patients.


The Australian difference


Macquarie University researchers led by Professor Andrew Georgiou from the Australian Institute of Health Innovation set out to change that by analyzing millions of patient records from general practitioners (GPs) in Sydney and Melbourne.

"Improving our understanding of long COVID, including who is being diagnosed, is vital to enhancing patient access to appropriate care, services and treatment," Professor Georgiou says.

Overseas research suggests demographic factors and pre-existing conditions as potential risk factors of long COVID.

But Professor Georgiou said Australians experienced the pandemic differently from most other countries, with the majority of exposure to COVID occurring after vaccination and predominantly from the omicron variant. This unique context suggests Australia should have a lesser burden of long COVID than overseas, but there is a lot more we need to find out, he says.

The study of 7 million medical records found that in Australia, patients with long COVID are more likely to be women than men, or were middle-aged, mostly living in a high socioeconomic area or those with pre-existing health problems.

Mental health, respiratory conditions such as asthma or emphysema, cancer or musculoskeletal conditions such as arthritis were among the chronic health conditions found in patients diagnosed with long COVID.

Uncertainty in making and documenting a definitive long COVID diagnosis while evidence of the condition is still emerging suggests the study almost certainly underrepresented the prevalence of the illness.


Good records crucial


Professor Georgiou says GP practices are at the frontline of identifying and managing long COVID.

"General practice plays a critical role in Australia's response to long COVID, not least because that is the first place people go when they are unwell or concerned," he says.

GP and a co-author of the study, Associate Professor Chris Pearce, also says GPs have a crucial role in unlocking the mysteries of long COVID and providing better care to patients.

"We encourage GPs to listen to patients and to record symptoms of long COVID in medical records otherwise the condition will continue to be under-represented in health statistics," Associate Professor Pearce says.

"Better recording leads to better understanding and better treatments. GPs are at the forefront of managing long COVID and are struggling to understand this complex disease. The more information we have to help them, the better."

More information: Abbish Kamalakkannan et al, Factors associated with general practitioner-led diagnosis of long COVID: an observational study using electronic general practice data from Victoria and New South Wales, Australia, Medical Journal of Australia (2024). DOI: 10.5694/mja2.52458
Journal information: Medical Journal of Australia
Provided by Macquarie University
 

Heliobas Disciple

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Study reveals stubborn mistrust in COVID-19 vaccine science
by CUNY Graduate School of Public Health and Health Policy
November 4, 2024


study-reveals-stubborn.jpg

Vaccine acceptance and willingness to take future recommended boosters by trust in science in 2023. Values represent percentages of N = 1,000 respondents. Credit: Vaccine: X (2024). DOI: 10.1016/j.jvacx.2024.100576


A study conducted by researchers from the CUNY Graduate School of Public Health and Health Policy (CUNY SPH) and the Barcelona Institute for Global Health (ISGlobal) sheds light on public trust in COVID-19 vaccine science and its impact on vaccine acceptance in the United States from 2021 to 2023.

The study is published in the journal Vaccine: X.

Analyzing data from a cross-sectional survey conducted in 2021, 2022, and 2023, the researchers found that around one-third of respondents expressed mistrust in the science behind COVID-19 vaccines (36.1% in 2021, 32.8% in 2022, and 36.2% in 2023).

Individuals who lost a family member or close friend to COVID-19 were significantly more likely to trust vaccine science and accept vaccination. Those who experienced a loss within the past year were nearly four times more likely to trust science compared to those who did not experience loss.

Higher trust levels were associated with male respondents, those with university degrees, and individuals with above-median incomes.

Trust in science was a strong predictor of vaccine acceptance and willingness to receive future boosters. Trust in the Centers for Disease Control and Prevention (CDC) as an information source was significantly correlated with both vaccine acceptance and future booster uptake.

"Our findings underscore the critical role of trust in science during public health crises," says ISGlobal Postdoctoral Fellow Trenton M. White, the study's lead author. "The fact that personal experiences of loss due to COVID-19 were associated with trust levels highlights the need for public health communications to be sensitive to the emotional impact of the pandemic."

The researchers emphasize that maintaining and enhancing public trust in vaccination programs requires strengthening trust in health communication from public sources, particularly the CDC. They suggest that future public health strategies should consider the diverse socio-economic and educational backgrounds of the U.S. population to effectively build and maintain trust in science-based solutions.

"This research provides valuable insights for policymakers and health communicators as they continue to navigate the ongoing challenge of global vaccine hesitancy," says CUNY SPH Dean Ayman El-Mohandes, the study's senior author.

More information: Trenton M. White et al, Trust in the science behind COVID-19 vaccines as a driver of vaccine acceptance in the United States, 2021–2023, Vaccine: X (2024). DOI: 10.1016/j.jvacx.2024.100576
Provided by CUNY Graduate School of Public Health and Health Policy
 

Heliobas Disciple

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The Heart Under Siege: New Insights Into Long COVID’s Lasting Impact
By University of Queensland
November 4, 20241

University of Queensland researchers have found that inflammatory proteins may be responsible for the lingering heart symptoms experienced by many long COVID patients.

The team discovered elevated cytokines—proteins involved in inflammation—in blood samples from people nearly a year and a half after their COVID infections. Lab tests showed that even trace amounts of these proteins could affect the cells responsible for the heart’s pumping ability.


Inflammatory Markers in Long COVID Patients

Research led by the University of Queensland has identified inflammatory markers in the blood of long COVID patients, offering potential insights into why many continue to experience cardiovascular issues.

Associate Professor Kirsty Short explained that the research aimed to uncover the causes of persistent chest pain and heart palpitations reported by long COVID sufferers.


Cytokines’ Impact on Heart Cells

“We discovered elevated levels of cytokines, proteins which help control inflammation in the body, in the blood samples of people at about 18 months post-infection with SARS-CoV-2,” Dr. Short said.

“Lab studies showed these trace-level cytokines had a direct effect on the functionality of cardiomyocytes, the cells of the heart responsible for its pump function.

“These particular types of cells are fundamental building blocks for our heart, so damaging them can lead to cardiovascular symptoms.”


Chronic Inflammation and Long-Term Symptoms

Dr. Short added that, until now, the role of chronic inflammation in causing cardiovascular symptoms had been unclear, particularly for those with symptoms lasting over a year post-infection.

The study examined blood samples from 50 participants across Australia, including those with long COVID symptoms for more than a year, individuals who had recovered from COVID, and those who had never been infected.


Nanotechnology Uncovers Trace Markers

The researchers used ‘immuno-storm chip’ nanotechnology developed at UQ’s Australian Institute for Bioengineering and Nanotechnology (AIBN) to discover trace elevated cytokines in the long COVID cohort, along with cardiac tissue damage markers measured at single-molecule resolution in blood.

“It’s only early days and these results require validation in additional patient cohorts, including those infected with more recent SARS-CoV-2 strains,” Dr. Short said.

“We’re now curious to know whether our findings could be applied to other symptoms of long COVID such as neurological disease or respiratory disease, as this study actively recruited sufferers with chest pain and/or heart palpitations.

“Despite these limitations, this work offers some important new insights into this complex disease, and hopefully offers opportunities to improve the diagnosis, treatment and understanding of long COVID.”


Collaborative Research Efforts

The research was led by UQ PhD candidates Jane Sinclair from the School of Chemistry and Molecular Biosciences (SCMB), Courtney Vedelago from AIBN, and Dr. Feargal J. Ryan from the South Australian Health and Medical Research Institute.

The research was a collaboration involving UQ’s SCMB, School of Mathematics and Physics, AIBN, Institute for Molecular Bioscience and Faculty of Medicine as well as the South Australian Health and Medical Research Institute, Flinders University, the University of Adelaide, the Australian National University, Mater Health Queensland, Mater Research Institute – UQ and QIMR Berghofer Medical Research Institute.

The samples for the research were provided by the COVID OZGenetics study, the Central Adelaide Health Network and the David Serisier Research Biobank at Mater Research.

The research paper was published in Nature Microbiology.

Reference: “Post-acute sequelae of SARS-CoV-2 cardiovascular symptoms are associated with trace-level cytokines that affect cardiomyocyte function” by Jane E. Sinclair, Courtney Vedelago, Feargal J. Ryan, Meagan Carney, Meredith A. Redd, Miriam A. Lynn, Branka Grubor-Bauk, Yuanzhao Cao, Anjali K. Henders, Keng Yih Chew, Deborah Gilroy, Kim Greaves, Larisa Labzin, Laura Ziser, Katharina Ronacher, Leanne M. Wallace, Yiwen Zhang, Kyle Macauslane, Daniel J. Ellis, Sudha Rao, Lucy Burr, Amanda Bain, Anjana Karawita, Benjamin L. Schulz, Junrong Li, David J. Lynn, Nathan Palpant, Alain Wuethrich, Matt Trau and Kirsty R. Short, 30 October 2024, Nature Microbiology.
DOI: 10.1038/s41564-024-01838-z
 

Heliobas Disciple

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U.S. CDC Now Reports That 7 Percent of Tested Dairy Farmworkers Were Possibly Infected with the H5N1 Virus
Nikhil Prasad Fact checked by:Thailand Medical News Team
Nov 08, 2024

The United States Centers for Disease Control and Prevention (CDC) recently published a study revealing that approximately 7% of tested dairy farmworkers might have been infected with the H5N1 avian influenza virus. Conducted in collaboration with the Michigan Department of Health and Human Services (MDHHS) and the Colorado Department of Public Health and Environment (CDPHE), the investigation focused on dairy farmworkers exposed to herds with confirmed H5N1 cases. Researchers aimed to evaluate the potential transmission of this virus from cattle to humans and to understand related health risks for workers.

This Medical News report delves into the key findings and broader implications of the U.S. CDC’s recent serologic study, which was carried out from June to August 2024 on dairy farms in Michigan and Colorado. The study presents significant data that could influence public health policy and the way farmworkers interact with animals infected by avian influenza viruses.


Details of the Study
In early 2024, highly pathogenic avian influenza (HPAI) A(H5) viruses were detected in the United States within dairy cattle, a previously unrecognized animal host. These infections raised concerns about potential transmission to humans, especially farmworkers directly handling these animals. The CDC's study sampled 115 dairy farmworkers across Michigan and Colorado, where HPAI A(H5) infections had been confirmed among dairy cattle. Blood samples were taken to test for antibodies against the virus, and the workers were also interviewed about their recent health, work duties, and use of personal protective equipment (PPE).

The study found that 7% of tested workers showed antibodies indicating recent exposure to the H5N1 virus. Most of these individuals were involved in tasks such as milking cows or cleaning milking parlors, which placed them in close contact with potentially infected animals. Notably, the majority of seropositive individuals reported mild or no symptoms during the exposure period, indicating that some H5N1 infections might go unnoticed due to their mild nature.


Key Findings on Transmission and Exposure
While past HPAI infections in humans have primarily been linked to poultry, the CDC’s report is one of the first to suggest the possibility of dairy cattle acting as an intermediate host for the virus. This development could increase the potential risk to workers on dairy farms, particularly those who interact closely with cows.

The study highlighted several critical insights into transmission risk. Workers who cleaned milking parlors, where virus-contaminated milk or respiratory secretions might be present, faced a notably higher risk. All seropositive individuals reported cleaning or milking tasks, while few of them recalled any direct physical symptoms at the time of exposure. This finding emphasizes the need for heightened surveillance and enhanced protective measures for dairy workers who frequently handle potentially infected animals.


Importance of Personal Protective Equipment (PPE)
One striking result from the study was the minimal use of recommended PPE among dairy farmworkers, even after confirmed cases of HPAI infections in their herds. CDC guidelines suggest that workers in close contact with infected animals wear eye and respiratory protection. However, fewer than 40% of workers used eye protection, and only 21% used respiratory masks such as N95 respirators.

This lack of PPE adherence, especially in environments where workers handle potentially infected milk or animal waste, could be a significant factor in the virus's transmission risk. The CDC has emphasized the importance of reinforcing PPE use, especially for tasks like cleaning, which may expose workers to higher viral loads. Enhanced training and accessible protective equipment may help prevent future transmission to workers.


Health Implications and Monitoring

The study reported mild symptoms in many workers, including red, itching eyes, sore throats, and occasional respiratory issues. Among those with antibodies, about half reported some symptoms, but none showed signs of severe illness. Previous studies on avian influenza viruses suggested that some strains could cause severe respiratory disease in humans. The current findings, however, suggest that many H5N1 infections in dairy workers might be asymptomatic or present with only mild symptoms.

This pattern of mild or absent symptoms complicates disease monitoring efforts. Workers may not recognize the need to report minor symptoms or seek medical attention. Public health authorities may thus need to adopt more proactive health monitoring on affected farms to detect cases early, including routine screenings for mild symptoms in workers exposed to infected herds. Such measures could help reduce the spread of the virus and prevent escalation to more severe disease.


Broader Public Health Implications
The CDC study underscores the urgent need for effective public health measures to prevent HPAI transmission among humans. While dairy farmworkers may not have shown severe illness, any case of zoonotic transmission (animal to human) raises concerns about viral adaptation and potential mutations that could enable easier human-to-human transmission.

The study suggests that regular surveillance of dairy herds for HPAI and public health outreach on farms are crucial for early identification of infected herds. Rapid detection of infected cattle and timely monitoring of exposed workers can mitigate transmission risks. Educational efforts tailored to farmworkers - often non-English speakers - should include clear guidance on using PPE and recognizing HPAI symptoms.


Conclusion
The CDC’s findings serve as a critical reminder of the need to bolster biosecurity and disease monitoring measures in animal husbandry industries. The evidence of H5N1 virus exposure among dairy farmworkers highlights a potential public health concern. Moving forward, implementing better protective measures, increasing PPE accessibility, and enhancing educational outreach to farmworkers could be key steps in minimizing zoonotic transmission risks.

The study findings were published in the peer-reviewed journal: Morbidity and Mortality Weekly Report.

 

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Your Nose Knows: Nasal Swab Test Predicts COVID-19 Severity
By Emory Health Sciences
November 6, 2024

New research from Emory University reveals that nasal autoantibodies in COVID-19 patients may help predict disease severity, with potential implications for treatment.

COVID-19 symptoms vary widely, from mild to severe. While current virus strains tend to cause milder cases, people with underlying health conditions remain at a significantly higher risk for severe illness. New research from Emory University is now offering a way to better predict the severity of COVID-19 by analyzing autoantibodies in the nasal cavity, potentially enabling more personalized treatment approaches. For those at high risk, this insight could guide immediate treatments, such as using medications like Paxlovid within a week of symptoms to reduce the chances of severe outcomes.

Published today (November 6) in Science Translational Medicine, the study followed 125 COVID-19 patients with mild to severe cases over nearly two years. Researchers monitored antibodies in both blood and nasal passages, discovering that over 70% of those with mild or moderate COVID-19 had specific autoantibodies in their nasal cavity. Interestingly, these nasal autoantibodies were linked to milder symptoms, stronger antiviral immune responses, and faster recovery.


Protective Role of Nasal Autoantibodies

The study suggests that nasal autoantibodies may play a protective role by helping to regulate the immune system, reducing excessive inflammation, and enhancing the body’s ability to fight the virus effectively.

“Generally, autoantibodies are associated with pathology and a negative prognosis, causing increased inflammation that would indicate more severe disease,” says Eliver Ghosn, senior author on the paper and faculty member of the Lowance Center for Human Immunology and Emory Vaccine Center. “What’s interesting about our findings is that with COVID-19, it’s the opposite. The nasal autoantibodies showed up soon after infection, targeting an important inflammatory molecule produced by the patient’s cells. These autoantibodies latched on to the molecule, likely to prevent excessive inflammation, and faded as people recovered, suggesting the body uses them to keep things in balance.”


Surprising Differences Between Blood and Nasal Responses

Previous studies on COVID-19 patients have suggested that autoantibodies in the blood predispose them to life-threatening disease. However, these studies often neglect the nose – the actual site of infection. The new study suggests that the immune responses mounted in the nose against the virus differ from those in the blood. In short, nasal autoantibodies equal protection, whereas autoantibodies found in the blood equal severity.

“The key to this puzzle was to look directly at the site of infection, in the nose, instead of the blood,” says Ghosn. “While autoantibodies in the blood were linked to bad prognosis, producing them only in the nose soon after infection is linked to efficient recovery.”


FlowBEAT: Innovation in Antibody Measurement

To allow more precise measurements of antibodies produced locally in the nasal site of infection, the Ghosn lab developed a new biotechnology tool called FlowBEAT to quantify different types of antibodies in nasal cavities and other biological samples, which could soon have implications for the testing of other respiratory viruses, like flu or RSV.

“Historically, the technology to measure antibodies has low sensitivity and is inefficient since they are limited to measuring one or a few antibodies at a time,” says Ghosn. “With FlowBEAT, we can take any standard nasal swab and perform a combination test to simultaneously measure all human antibody types against dozens of viral and host antigens in a single tube – a much more sensitive, efficient, and scalable way to measure for autoantibodies in the nose that can also predict the severity of symptoms.”


Implications for Other Respiratory Infections

Next, the researchers want to find out whether this surprising mechanism to control COVID-19 infection in the nose also plays a role in other respiratory infections like flu and RSV.

“If this nasal autoantibody response turns out to be a common mechanism to protect us against other viral infections, it can be a paradigm shift in how we study protective immunity,” says Ghosn. “We will interpret autoantibodies through an innovative lens, hopefully inspiring new lines of research and better therapeutic options for common respiratory infections.”


Future of Diagnostic Testing for Respiratory Viruses

Based on their findings, the Ghosn Lab is currently working with Emory’s patent office to develop a predictive diagnostic tool using “leftover” samples from standard nasal swabs widely used as a diagnostic test for COVID-19.

“Right now, we’re either looking at infection risk before it happens or analyzing the infection course well after recovery,” says Ben Babcock, a PhD candidate who led the study in the Ghosn Lab. “Imagine if we could capture the immune response in real-time, right in the clinic. A just-in-time test could give physicians and patients the real-time information they need to make faster, smarter treatment decisions.”

Reference: “Transient anti-interferon autoantibodies in the airways are associated with recovery from COVID-19” by Babcock et al., 6 November 2024, Science Translational Medicine.

This study was part of a large collaboration between the Ghosn Lab at Emory and Drs. Sulggi Lee from UCSF and Nadia Roan from Gladstone Institutes, and in partnership with Emory laboratories of Drs. F. Eun-Hyung Lee, Iñaki Sanz, and Rabin Tirouvanziam.

This work was supported by the NIH’s National Institute of Allergy and Infectious Diseases (NIAID) awards R21AI167032, R01AI123126-05S1 and National Cancer Institute (NCI) award U54 CA260563 Emory SeroNet; COVID Fast Grant from Emergent Ventures at the Mercatus Center; and the Program for Breakthrough Biomedical Research Award. Ben Babcock was partially supported by the American Society of Hematology (ASH).
 

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US expands bird flu testing after finding symptom-free infections in people
By Deena Beasley and Leah Douglas
November 7, 2024 7:49 PM UTC

Nov 7 (Reuters) - Farm workers who have been exposed to animals with bird flu should be tested for the virus even if they do not have symptoms, the U.S. Centers for Disease Control and Prevention said on Thursday.

The change to the agency's testing recommendation comes as the U.S. Department of Agriculture is also expanding its testing of milk for bird flu, signaling concern by both agencies about the ongoing spread of the virus on dairy and poultry farms.

Bird flu has infected nearly 450 dairy farms in 15 states since March, according to USDA data.
The CDC is not seeing mutations in the virus that would lead to easier transmission or evidence of person-to-person spread, agency officials said on a press call.

The CDC has identified 46 human cases of bird flu since April, though farm worker groups have suggested the figure is an undercount as workers avoid testing for fear of economic repercussions from quarantining or because their symptoms are too mild to warrant concern.

Disease experts have warned that as the virus circulates, the risk of it more easily infecting humans increases, which could lead to a pandemic.

"There may be individuals who were infected with H5 but who do not recall having symptoms. That means that we in public health need to cast a wider net in terms of who is offered a test," Nirav Shah, CDC's principal deputy director, said on the call with reporters.

Recent testing of 115 dairy farm workers in Michigan and Colorado who were exposed to cows infected with H5N1 bird flu found that 7% of them had evidence of prior infection, but only half remembered having symptoms, according to a CDC study released on Thursday.

The June through August serological study found evidence of antibodies to the virus in eight workers involved in milking and cleaning milking parlors.

The CDC is also recommending offering the antiviral drug Tamiflu to workers with high risk exposures to sick animals and widening its guidance for worker protective equipment, including eye protection.

The USDA last week said it would begin testing bulk milk for bird flu after a push from industry and veterinary groups concerned about the virus' spread.

A pig on an Oregon farm tested positive for bird flu for the first time in the U.S. on Oct. 30, concerning virologists because pigs have been a source of prior human pandemics. The USDA said on Nov. 6 that a second pig on the farm had also tested positive.
 

Heliobas Disciple

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Posting this because the Mayo Clinic is now saying you don't even get 3 months of natural immunity from having Covid. This is the exact opposite of what Geert says. There are different types of immunity, which one is each talking about? I think that may be the discrepancy. I side with Geert on this... Unless of course the Mayo Clinic is referring to the Vaxxed. On that point I agree, and I would think Geert would too.... Of course, I'm not a dr or a medical expert. Geert is though;)



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Mayo Clinic Minute: 3 misconceptions about COVID-19 and flu vaccines
DeeDee Stiepan
November 7, 2024

Misconceptions about the influenza and COVID-19 vaccines may make some people hesitant to roll up their sleeves. What better way to clear up the confusion than hearing straight from a Mayo Clinic expert?

In this Mayo Clinic Minute, Dr. Robert Jacobson, medical director for Mayo Clinic's Primary Care Immunization Program, clears up some misconceptions about COVID-19 and the flu.

1 min 5 sec
View: https://www.youtube.com/watch?v=WGcqiTAR5hY


Misconception #1: The flu and COVID-19 vaccines can make you sick.

"You aren't going to get the flu from the flu vaccine. You're not going to get COVID from the COVID vaccine. It may feel momentarily like you're coming down with something, but it's going to resolve without any treatment," says Dr. Jacobson.

Misconception #2: Supply issues.

Some may worry about supply issues and don't want to take vaccines away from other who may really need them. Dr. Jacobson says, while that may have been the case when the COVID-19 vaccine was first rolled out, it's not anymore.

"We have three manufacturers in this country making COVID-19 vaccines (which) are licensed or approved for use by the FDA, and monitored and recommended by the ACIP (Advisory Committee on Immunization Practices). Pharmacies, healthcare organizations and public health have the vaccines available for you. That's not an excuse," says Dr. Jacobson.

Misconception #3: Natural immunity from a recent infection.

Finally, some may believe they don't need vaccination because they had a recent infection. However, Dr. Jacobson explains why you can't rely on natural immunity alone.

"Not everybody, who even has a good immune system, gets three months protection out of it. We're not in a situation where our resources are strained to get you the COVID vaccine. So you no longer have to do us the favor and wait the three months," says Dr. Jacobson.

The truth:

Getting vaccinated for the flu and COVID-19 is the best way to keep yourself and the people around you safe from infection.
 

Heliobas Disciple

TB Fanatic
This is on Geert's page and not behind a paywall so he must want it read and passed around. Geert is generally pro-vaxxed so it's not surprising that he would write something like this. Maybe disappointing in some ways, although there are some vaccines that did work and did save lives so it's not a black and white, all or none situation. I think RFK would agree, he has repeatedly said he's not anti-vaxx, he just wants to make sure they work and are safe. Don't we all?


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My message to RFK Jr.: Think carefully before acting on your new vaccine policy.
Geert Vanden Bossche
Nov 08, 2024

The outcome of the U.S. election, with RFK Jr. overseeing public health issues, will bring about a spectacular shift in public health policy. This is a welcome change, as the incompetence, conflicts of interest, and stubbornness of health authorities in the U.S. and beyond are disheartening. However, as a vaccinologist, I am somewhat concerned about the extreme polarization that America is currently experiencing. This polarization now threatens to penetrate even the deepest layers of society, including public health.

For every point of disagreement, the response nowadays seems to need to be black or white. These days, one is either an unconditional advocate of unrestricted vaccination practices or despises every needle that fits on a vaccine syringe. The scientific weighing of pros and cons—depending on the target group, type of vaccine, epidemiological situation, and objective data from relevant studies—seems to no longer be part of the decision-making process for many.

Often, arguments regarding the isolated impact on the individual are overly simplistic. I don’t mean to suggest that we, as a society, should just have to accept that our healthy children—who may never even become exposed to the disease they are being vaccinated against—being injected with substances that could potentially cause serious health issues, even if the latter would only occur on very rare occasions. Rather, I am referring to the general lack of awareness that so-called vaccine-preventable infectious diseases can only be contained through a form of immunity collectively mounted by the population, namely, herd immunity. This has become a topic that neither the so-called pro- nor anti-vaxxers wish to debate, likely because few truly understand its biological implications. I recently pointed out some common misunderstandings regarding this issue:


Herd immunity ensures that the spread of the virus is suppressed to the point where it no longer causes productive infections in individuals who lack protective immunity to the virus. Herd immunity can only be achieved when a large enough portion of the population builds an immune response that protects against productive infection. Such immunity develops spontaneously when, for example, a population is overwhelmed by a pandemic caused by a virus that naturally provokes an acute, self-limiting infection. Such viral infections (e.g., SARS-CoV-2) can spread rapidly through asymptomatic shedding but are usually quickly contained by cytotoxic immune effector cells in individuals who develop symptomatic infection (hence, the self-limiting nature of these infections).

Symptomatically infected individuals are protected from productive infection upon subsequent exposure, thanks to trained innate immunity, which may be combined with a recall of previously induced, virus-neutralizing antibodies (Abs). Consequently, larger portions of the population will eventually have sterilizing immunity after natural infection. In many cases, especially among children and young healthy people, a well-trained first line of immune defense as the sole natural immune response suffices to prevent productive infection upon exposure. This already explains why in a young and healthy population, the level of herd immunity cannot be assessed by measuring the increase in serum titers of (neutralizing) Abs. Such measurement of so-called seroconversion in the population would lead to a serious underestimation of herd immunity. Conversely, when virus spread is controlled by herd immunity, innate immunity will weaken, and neutralizing Ab concentrations in the blood will decrease, reducing herd immunity. This, however, is not a problem as long as the population is not exposed to an external source of the virus, or a sufficient portion of the population possesses an immunological memory of neutralizing Abs. However, individuals who have not previously contracted the disease or didn’t even get infected at all are at risk of becoming ill, or even severely ill, when herd immunity wanes. This is why and how maintaining herd immunity can prevent recurrent epidemics.

Immunizing the immunologically naive portion of the population (e.g., newborns) with live-attenuated vaccines not only strengthens innate immunity but also establishes an immunological memory of adaptive Abs, thereby contributing both to the individual protection of the vaccinated and to maintaining herd immunity in the population. While maintaining herd immunity can prevent recurrent epidemics, it cannot prevent a pandemic caused by a highly divergent viral variant due to the specificity of the Abs produced by previously infection- or vaccine-induced memory B cells. It is therefore not surprising that these live-attenuated vaccines can only be used to prevent epidemics caused by specific viruses that not only provoke acute, self-limiting infections but also have a high degree of genetic stability (e.g., measles, mumps, rubella virus).

I therefore continue to advocate for a new vaccine approach that enables training of broad, non-variant-specific cell-mediated innate immunity to prevent productive infection through sterilizing immunity. Such an immune intervention would not only protect the vaccinated individual from illness but also protect immunologically naive individuals by sufficiently curbing virus transmission within the population to prevent productive infection in these individuals.

I therefore continue to argue that a laissez-faire attitude toward viruses capable of rapidly spreading through entire populations and causing acute, potentially fatal infections is a flawed approach, as it will create gaps in the population's herd immunity. Even in industrialized countries, good general and personal hygiene and adequate sanitary conditions cannot guarantee protection against these viruses, especially when they are also airborne. Large gaps in herd immunity can quickly lead to high infection pressure, where it is even conceivable that the virus could cause severe breakthrough infections in immunologically primed individuals.

There are indeed approaches with the potential to enhance natural, cell-based innate immunity (e.g., Natural Killer cell vaccines) in a way that provides broad protection against a multitude of respiratory viruses and other infectious agents (or even non-infectious agents like allergens). However, it goes without saying that the vaccine industry is not interested in developing such broad-spectrum vaccines as deploying immune interventions that can prevent or treat multiple diseases/infections simultaneously does not represent a lucrative objective. On the other hand, the notion that we should throw out the baby with the bathwater and focus solely on personalized vaccinology, even for infectious diseases that manifest at a population level, is at best short-sighted.
 

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Discovery of rapid COVID-19 replication mechanism could expand treatment options

by National Research Council of Science and Technology
November 6, 2024


discovery-of-rapid-cov.jpg

A schematic diagram showing the significant contribution of SCoV2-induced altered mitochondrial dynamics and mitochondrial EGFR translocation in sustaining viral propagation. First, SCoV2 RNA and nucleocapsid complex increases membrane potential during the early stages of SCoV2 infection. This alteration subsequently promotes mitochondrial elongation. SCoV2 also activates the mitochondrial OXPHOS process, thereby promoting ATP production. Second, SCoV2 activates EGFR-mediated cell survival signaling and subsequently promotes mitochondrial EGFR internalization, which contributes to the maintenance of abnormal mitochondrial bioenergetics. These alterations are physiologically relevant to the maintenance of homoeostasis of SCoV2-infected cells and robust SCoV2 propagation. Credit: Korea Research Institute of Chemical Technology (KRICT)


Concerns about COVID-19 have significantly diminished, but researchers continue to analyze its high transmission rate, aiming to prepare for future infectious diseases. A research team has newly identified the mechanism behind the rapid proliferation of the COVID-19 virus.

Dr. Seong-Jun Kim's team from the Korea Research Institute of Chemical Technology (KRICT) have reported in a research paper that the rapid proliferation of COVID-19 is due to altered roles of mitochondria and epidermal growth factor receptor (EGFR; responsible for growth signal transmission in cells).

The paper is published in the journal Signal Transduction and Targeted Therapy.

Pandemic-causing coronaviruses, such as SARS in 2003, MERS in 2015, and COVID-19 in 2019, have been repeatedly emerging. Given the increasing frequency of such outbreaks, there is an urgent need to accelerate the response to new infectious diseases.

While numerous studies on COVID-19 have been conducted, focusing initially on the viral entry mechanism and vaccine development, recent research has explored methods to hinder viral replication by altering calcium ion concentrations in cells.

However, the precise mechanism underlying the rapid replication of the virus after it enters human cells has remained unclear. Understanding this process is crucial for future pandemic preparedness.

Dr. Kim's team revealed that once COVID-19 invades human cells, it quickly modifies the structure and function of mitochondria to abnormally enhance energy production, which is essential for viral replication. They also discovered that the virus manipulates the EGFR protein, which is critical for cellular growth signaling, to maintain this rapid replication.

This increases the likelihood of the virus replicating and spreading in large numbers. Importantly, the team demonstrated through experiments that using EGFR-targeting drugs could effectively treat COVID-19.


discovery-of-rapid-cov-1.jpg

Lung tissue qRT-PCR test results three days after administration - Viral RNA reduced approximately 10-fold. The results of a staining test on the lung tissue inflammation area six days after administration, ? Significantly alleviates lung inflammation. Credit: Korea Research Institute of Chemical Technology (KRICT)


The researchers focused on two major phenomena occurring after the virus enters host cells:
  • Enhanced ATP production: The viral RNA-nucleocapsid complex influences the mitochondrial membrane potential, leading to abnormal increases in energy production. Mitochondria fusion is promoted, increasing surface area and ATP production efficiency.
  • Alteration of EGFR function: COVID-19 infection activates the EGFR signaling pathway, with altered EGFR relocating to mitochondria. This sustains excessive energy production, facilitating rapid viral replication.

Using FDA-approved EGFR inhibitors, such as vandetanib and dacomitinib, the team confirmed significant antiviral effects. Notably, vandetanib was highly effective, reducing viral RNA levels in infected mice by 90% after oral administration for three days and significantly alleviating lung inflammation after six days.

Additionally, the antiviral efficacy of vandetanib against COVID-19 variants such as alpha, beta, delta, and omicron was remarkable, with as much as a 100,000-fold reduction of viral RNA levels in some cases. Vandetanib also effectively prevented the infection of newly produced viral progeny.

The results demonstrate a novel mechanism underlying COVID-19's rapid replication and suggest the potential for drug repurposing to treat viral infections using existing approved therapies. This discovery could be a significant step toward combating future infectious diseases.

Dr. Kim from the KRICT said, "At a time when we need to prepare for the frequent spread of infectious diseases, the identification of a new mechanism for rapid viral replication and the development of new treatment strategies will contribute to the health and safety of people."

More information: Hye Jin Shin et al, SARS-CoV-2 aberrantly elevates mitochondrial bioenergetics to induce robust virus propagation, Signal Transduction and Targeted Therapy (2024). DOI: 10.1038/s41392-024-01836-x
Provided by National Research Council of Science and Technology
 

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ETA: I am switching out the article I originally posted on this story with the one below because the first one was vague and didn't give the actual details and this one gives more concrete information.


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EMPHASIS MINE

Jury awards $12M to woman fired for refusing COVID vax. Hundreds of similar suits pending.
JC Reindl Detroit Free Press
Published 6:09 p.m. ET Nov. 8, 2024 Updated 10:07 p.m. ET Nov. 8, 2024

A longtime employee of Blue Cross Blue Shield of Michigan who was fired after refusing for religious reasons to get the COVID-19 vaccine has been awarded more than $12 million by a federal jury.

The jury in Detroit returned the verdict Friday afternoon, finding that Blue Cross discriminated against Lisa Domski, of Wyandotte, who is Catholic, by denying her an exemption to its companywide vaccine mandate, an exemption she had sought based on her "sincerely held religious belief."

Denying her that exemption, known as an accommodation, was a violation of federal and state law, the jury found. They awarded Domski a total of $12.69 million, or $315,000 for back pay, $1.375 million for forgone future wages, $1 million for noneconomic damages and $10 million in punitive damages

Her attorney, Jon Marko of Marko Law in Detroit, said Domski's lawsuit against Blue Cross was the first of its kind to go to trial in Michigan involving an employer denying a religious accommodation to a COVID-19 vaccine mandate.

In a similar case last month in San Franciso, a federal jury awarded more than $1 million each to six Bay Area Rapid Transit agency workers who also didn't get the vaccine for religious reasons.

Domski had worked at Blue Cross for 32 years, most recently in IT. Blue Cross terminated her employment on Jan. 5, 2022, which was the deadline for all Blue Cross employees and contractors — including those working remotely — to be fully vaccinated against COVID-19.

Domski had sought a religious exemption out of her belief that the three COVID-19 vaccines in wide use at the time — by Pfizer, Moderna and Johnson & Johnson — were all either developed or tested using fetal cells that originated in abortion, and she thought it would be a sin to inject her body with such a vaccine because abortion is wrong.

“She was working from home, she didn’t pose a danger to anyone else, and she had a sincerely held religious belief against the use of the vaccine," Marko told the Free Press on Friday. “Blue Cross, what they did was evil.”

According to a Michigan Department of Health and Human Services fact sheet, although the initial three COVID-19 vaccines didn't contain fetal cells, the Johnson & Johnson vaccine was indeed developed and manufactured by growing the virus in fetal cells, and a fetal cell line was used early on for testing the Pfizer and Moderna mRNA vaccines.

Blue Cross may appeal the verdict. In a statement released Friday afternoon, the insurer said it is reviewing its legal options and will determine its next step in the coming days.

"Throughout the pandemic, Blue Cross Blue Shield of Michigan, together with its employees, worked to promote the health and safety of our colleagues, stakeholders, and communities," the statement said. "As part of that shared work, in October 2021, Blue Cross, and its subsidiaries, enacted a vaccine policy requiring all of its employees to be fully vaccinated for Covid-19 or obtain a religious or medical accommodation.

"In implementing the vaccine policy, Blue Cross designed an accommodation process that complied with state and federal law and respected the sincerely held religious beliefs of its employees. While Blue Cross respects the jury process and thanks the individual jurors for their service, we are disappointed in the verdict."

Marko said he represents clients in nearly 180 similar cases against Blue Cross Blue Shield of Michigan or its subsidiaries.

"This is going to set the tone for Blue Cross, because it’s only going to get worse for them from here on out," he said.
Marko said that he, too, is Catholic but voluntarily chose to get vaccinated, so he was initially a bit skeptical about the lawsuit.

“But as I really got into the case and I got to know what Blue Cross did to these loyal workers, I knew I had to do something about it," he said.

Domski's lawsuit, filed in August 2023 in U.S. District Court in Detroit, accused Blue Cross of violating the 1964 Civil Rights Act, which requires employers to make reasonable accommodation for an employee's religious beliefs and practices. It also claimed discrimination and disparate treatment under Michigan's Elliott-Larsen Civil Rights Act.

According to court documents, Blue Cross argued that Domski's request for an accommodation didn't meet the criteria for a religious exemption. The insurer tried to conduct an interview with her in December 2021, but she declined to answer the interviewer's questions, saying she would instead rely on a written statement she had submitted.

"My religious view has always been and continues to be that abortion is murder and a sin against God," Domski wrote in the statement. "I must consider the moral aspects of the use of all vaccines that have connection to fetal cell lines obtained from an abortion."

According to Domski's lawsuit, the senior Blue Cross employee in charge of deciding who could get an exemption to the vaccine mandate had told colleagues that he doubted the validity of any religious accommodation request.

Blue Cross ultimately rejected 75% of all the religious accommodation requests, according to the lawsuit, leading to termination of 250 employees in January 2022.

Blue Cross conducted interviews with employees seeking such accommodations, lasting up to 15 minutes and involving 10 primary questions.

One of the questions was whether the employees took the over-the-counter medicines aspirin, Sudafed, Tums or Tylenol, and the employees were told — erroneously — that Tylenol and Tums were developed and manufactured using stems cells, according to Domski's lawsuit.

Ann Arbor attorney Noah Hurwitz of Hurwitz Law is co-counsel with Marko in Domski's case.

Hurwitz said he is also involved in 300 or so other lawsuits brought by workers who were fired from their jobs for not getting COVID-19 vaccines. Hurwitz said all of those individuals were denied either a religious or medical exemption.

The other employer defendants include T-Mobile, Carhartt, Honeywell, Henry Ford Health, Ascension Health, Trinity Health, MotorCity and MGM Grand casinos in Detroit and the city of Ann Arbor.

About 90% of the cases that so far have reached a conclusion ended in settlements, he said, and a majority of those cases centered on religious accommodations.

The medical accommodations cases can be tough to win, Hurwitz said, as they typically require having a qualifying disability under the Americans with Disabilities Act. So even a doctor's note saying that an employee had bad reactions to other vaccines in the past can be insufficient to get out of an employer's COVID-19 vaccine mandate, he said.

Hurwitz said he knows of health systems that require annual flu vaccines for all of their employees, even though flu shots are well below 100% effective, because they wish to avoid a mass outbreak situation in which all hospital staff get sick at once. Those types of vaccine mandates have been upheld in court, he said.
 
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Did COVID Lockdowns Drive a Flu Strain to Extinction?
By Walter Beckwith, American Association for the Advancement of Science (AAAS)
November 7, 2024

During the COVID-19 pandemic, global influenza cases dropped dramatically due to lockdowns and travel restrictions. However, in regions with fewer restrictions, influenza continued to circulate, fueling its evolution.

Research shows that global air travel is key to influenza spread, and while many lineages returned post-pandemic, influenza B/Yamagata may have gone extinct.

During the COVID-19 pandemic, travel restrictions and social measures led to a sharp worldwide decrease in seasonal flu cases. However, certain influenza strains continued to circulate and evolve in regions with fewer restrictions, particularly in tropical areas like South and West Asia. The spread of seasonal flu is strongly influenced by social behaviors, especially air travel, and by the periodic emergence of new strains that evade immunity from previous infections or vaccinations.

In 2020, nonpharmaceutical interventions (NPIs) aimed at controlling COVID-19—such as lockdowns, mandated social distancing, masking, and travel bans—significantly disrupted influenza transmission and evolution. As a result, global cases of seasonal flu, including A subtypes H1N1 and H3N2 and B subtypes Victoria and Yamagata, saw a dramatic decline.

In this study, Zhiyuan Chen and colleagues investigated how these changes affected the spread, distribution, and evolutionary dynamics of seasonal influenza lineages. Using a phylodynamic approach, the researchers combined epidemiological, genetic, and international travel data from before, during, and after the COVID-19 pandemic and found that the onset of the pandemic led to a shift in the intensity and structure of international influenza transmission.

Although influenza cases significantly dropped globally during the pandemic’s peak, in South Asia and West Asia, regions that had relatively fewer pandemic restrictions, the circulation of influenza A and influenza B/Victoria lineages, respectively, continued. That circulation served as important evolutionary sources, or “phylogenetic trunk locations,” of influenza viruses during the pandemic period.

By March 2023, as global air traffic resumed, the circulation of influenza lineages returned to pre-pandemic levels, highlighting the virus’ resilience to long-term disruption and its reliance on global air travel patterns to spread. Notably, however, the findings also show that the influenza B/Yamagata lineage appears to have disappeared since the start of the pandemic, suggesting that the lineage may have since gone extinct.

“The study by Chen et al. further reinforces that nonpharmaceutical interventions can be incredibly effective in disrupting viral transmission, pathogen diversity, and antigenic evolution, and are arguably more effective than vaccine efforts alone,” write Pejman Rohani and Justin Bahl in a related Perspective.

Reference: “COVID-19 pandemic interventions reshaped the global dispersal of seasonal influenza viruses” 7 November 2024, Science.
DOI: 10.1126/science.adq3003
 

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Research points to correlation between preeclampsia and COVID-19 in pregnant women
by Maria Fernanda Ziegler, FAPESP
November 8, 2024

During the COVID-19 pandemic, above all before vaccines were available, an alarm was sounded regarding a possible correlation between severe cases of COVID-19 in pregnant women and preeclampsia, a condition characterized by high blood pressure (hypertension) in the expectant mother and high levels of protein in her urine (proteinuria). It can entail dangerous complications for mother and baby.

Preeclampsia was more frequent in pregnant women infected by SARS-CoV-2 and was associated with a heightened risk of complications and death.

Differential diagnosis was a major clinical challenge at the time. While gestational preeclampsia, which is most frequent in the third trimester, elevates the risk of kidney and liver failure as well as causing placental dysfunction and high blood pressure, so does severe COVID-19, owing to the exacerbated inflammation caused by the virus.

The protocols for treating the two conditions are different. In the case of preeclampsia, the pregnancy must be interrupted and the baby delivered as soon as possible by cesarean section, whereas in a woman with COVID-19 the pregnancy can proceed, with clinical support until the infection improves.

Assuring a correct diagnosis was even more important in severe cases of preeclampsia (known as HELLP syndrome), especially before the 34th week of pregnancy.

Three years after the most lethal period of the pandemic, a review of the scientific literature published in the American Journal of Reproductive Immunology emphasizes the pathophysiological similarities between preeclampsia and COVID-19.

The study was conducted by researchers at the State University of Campinas (UNICAMP) in São Paulo state, Brazil, and Baylor College of Medicine in Houston, Texas (U.S.).

The similarities highlighted in the article include shared pathways involving the renin-angiotensin system (a hormone system that plays a key role in regulating blood pressure and fluid balance in the body) and angiotensin-converting enzyme 2 (ACE2), the receptor to which SARS-CoV-2 binds to infect human cells.

Another study by the same group identified biomarkers that distinguish preeclampsia from severe COVID-19 in pregnant women.

"The two conditions do indeed have many similarities. Both severe COVID-19 and preeclampsia can involve multiple organ dysfunction and high blood pressure. There are also similarities in the mechanism, as ACE2 plays a key role in regulating blood pressure. It's possible therefore that COVID-19 heightens the risk of preeclampsia, as suggested by several studies that point to a higher frequency of preeclampsia in COVID-19 patients," Maria Laura Costa do Nascimento, last author of the review article and a professor of obstetrics at UNICAMP said.

More than 300 pregnant women die from preeclampsia in Brazil every year. High-income countries have all but eliminated this cause of death thanks to investment in actions to assure timely diagnosis and effective treatment, Nascimento said.

Maternal deaths rose very sharply during the pandemic. Data from the Ministry of Health show that 1,965 women died during or following pregnancy and childbirth in 2020. The number jumped to 3,030 in 2021. The same data also show a high risk of preeclampsia.

"Our goal for 2030 in terms of maternal mortality is to reach less than 30 deaths per 100,000 live births. Right now [based on data for 2023], we're at 70 deaths per 100,000 live births. During the pandemic, in 2021, the national average was 120, with higher numbers in some states and regions. COVID-19 magnified the preexisting trend and evidenced the impact of this condition on adverse outcomes," she said.

The rise in maternal mortality during the pandemic cannot be blamed on the rise in cases of preeclampsia. "This is due to lack of both epidemiological surveillance findings and a proper diagnosis of the condition," Nascimento said.

"What we can say, based on a multicenter study we conducted during the pandemic with data from 16 maternity hospitals across Brazil, is that the risk of death or severe disease increases when both conditions are present. Moreover, our review of the literature shows that the prevalence of preeclampsia rises among COVID-19 patients."


Biomarkers

Another study by Nascimento's group identified biomarkers that distinguished between preeclampsia and COVID-19 in pregnant women.

"They're classical markers of preeclampsia [proteins sFlt-1 and PlGF] that help control vasoconstriction and vasodilation. These proteins are produced by placenta cells throughout gestation. An imbalance is observed in cases of preeclampsia, with proangiogenic proteins [PIGF] diminishing and antiangiogenic proteins [sFlt-1] increasing," she said.

"We concluded that these biomarkers are specific for preeclampsia. They aren't altered in COVID, which could help assure a differential diagnosis."

There are well-established risk factors for preeclampsia, she added, especially chronic high blood pressure, having had preeclampsia in a previous pregnancy, expecting twins, having diabetes, and having an autoimmune disease.

"Several factors make close monitoring of all pregnancies advisable. COVID-19 may have to join the list in future," she said.

More information: Guilherme M. Nobrega et al, Preeclampsia in the Context of COVID-19: Mechanisms, Pathophysiology, and Clinical Outcomes, American Journal of Reproductive Immunology (2024). DOI: 10.1111/aji.13915
Provided by FAPESP
 

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SARS-CoV-2 'steals' our proteins to protect itself from the immune system, study reveals
by Medical University of Vienna
November 8, 2024


sars-cov-2-steals-our.jpg

Association of host cell-derived CD55 and CD59 with purified SARS-CoV-2 particles. Credit: Emerging Microbes & Infections (2024). DOI: 10.1080/22221751.2024.2417868

Researchers at the Medical University of Vienna and the Medical University of Innsbruck discovered that SARS-CoV-2 hijacks three important host proteins that dampen the activity of the complement system, a key component of early antiviral immunity.

This significantly impairs viral clearance which may affect the course of both acute COVID-19 infections and post-COVID-19 sequelae. The study is published in the journal Emerging Microbes & Infections.

An early and effective immune response is crucial for resolving viral infections and preventing post-infectious complications. The complement system, a pivotal element of antiviral immunity, is a cascade of proteins found in the bloodstream and at mucosal sites, such as the respiratory tract.

Activated through three different pathways, complement facilitates the clearance of virus particles by directly inducing their destruction (lysis). To prevent bystander damage to host cells, complement is rapidly inactivated by a set of host molecules referred to as complement regulatory proteins.

The study led by Anna Ohradanova-Repic and colleagues from the Center for Pathophysiology, Infectiology and Immunology at the Medical University of Vienna in collaboration with the team of Heribert Stoiber from the Institute of Virology at the Medical University of Innsbruck shows that SARS-CoV-2 hijacks three of these regulatory proteins, CD55, CD59 and Factor H, and thereby successfully shields itself from complement-mediated lysis.


Hijacking host proteins for effective complement resistance

By propagating SARS-CoV-2 in human cells, the researchers discovered that the virus particles acquire the cellular proteins CD55 and CD59. Further experiments showed that SARS-CoV-2 also binds to Factor H, another complement regulatory protein that is primarily found in the bloodstream.

Confronting the virus particles with active complement revealed that they are partially resistant to complement-mediated lysis. By removing CD55, CD59 and Factor H from the virus surface or inhibiting their biological functions, the researchers could successfully restore complement-mediated clearance of SARS-CoV-2.

"Through hijacking these three proteins, SARS-CoV-2 can evade all three complement pathways, resulting in reduced or delayed viral clearance by the infected host," Anna Ohradanova-Repic, the leader of the study explains.

Because complement is intricately linked with other components of the immune system, this not only affects virus elimination but can also cause significant inflammation, a core feature of both severe COVID-19 and long COVID.

"Uncovering immune evasion mechanisms that allow the virus to linger within the host for longer, deepen our understanding of the acute and long-term impacts of SARS-CoV-2 infection," says first author Laura Gebetsberger.

More information: Laura Gebetsberger et al, SARS-CoV-2 hijacks host CD55, CD59 and factor H to impair antibody-dependent complement-mediated lysis, Emerging Microbes & Infections (2024). DOI: 10.1080/22221751.2024.2417868
Provided by Medical University of Vienna
 

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COVID-19 linked to long-term risk for autoimmune, autoinflammatory disease
by Elana Gotkine
November 8, 2024

COVID-19 is associated with long-term risk for autoimmune and autoinflammatory connective tissue disorders, according to a study published online Nov. 6 in JAMA Dermatology.

Yeon-Woo Heo, M.D., from the Yonsei University Wonju College of Medicine in South Korea, and colleagues conducted a retrospective cohort study to examine the long-term risk for autoimmune and autoinflammatory diseases after COVID-19. The analysis included individuals with confirmed COVID-19 from Oct. 8, 2020, to Dec. 31, 2022 (3,145,388 patients) and controls who participated in the general health examination in 2018 (3,767,039 controls) with an observation period of more than 180 days.

The researchers found that COVID-19 was significantly associated with an increased risk for alopecia areata, alopecia totalis, vitiligo, Behçet disease, Crohn disease, ulcerative colitis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren syndrome, ankylosing spondylitis, and bullous pemphigoid (adjusted hazard ratios, 1.11, 1.24, 1.11, 1.45, 1.35, 1.15, 1.09, 1.14, 1.13, 1.11, and 1.62, respectively). Demographic factors, including male and female sex, age younger than 40 years, and age 40 years and older, showed diverse associations with the risk for autoimmune and autoinflammatory outcomes in subgroup analyses. Higher risk was also seen in association with severe COVID-19 infection requiring intensive care unit admission, the delta period, and not being vaccinated.

"Understanding the specific vulnerabilities and disease patterns among different subgroups is crucial for mitigating the long-term impact of the pandemic on global health," the authors write.

More information: Yeon-Woo Heo et al, Long-Term Risk of Autoimmune and Autoinflammatory Connective Tissue Disorders Following COVID-19, JAMA Dermatology (2024). DOI: 10.1001/jamadermatol.2024.4233

Lisa M. Arkin et al, COVID-19 as a Risk Factor For Autoimmune Skin Disease, JAMA Dermatology (2024). DOI: 10.1001/jamadermatol.2024.4222
Journal information: JAMA Dermatology
 

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Infection Aftershock: COVID-19’s Long-Term Impact on Your Heart
By National Heart, Lung, and Blood Institute (NHLBI)
November 10, 2024

New research indicates that people who contracted COVID-19 early in the pandemic faced a significantly elevated risk of heart attack, stroke, and death for up to three years post-infection.

Those with severe cases saw nearly quadruple the risk, especially in individuals with A, B, or AB blood types, while blood type O was associated with lower risk. This finding highlights long-term cardiovascular threats for COVID-19 patients and suggests that severe cases may need to be considered as a new cardiovascular risk factor. However, further studies on more diverse populations and vaccinated individuals are needed to validate these results.
Long-Term Cardiovascular Risks Linked to COVID-19 Infection

A recent study supported by the National Institutes of Health (NIH) found that COVID-19 infection significantly increased the risk of heart attack, stroke, and death for up to three years in unvaccinated people who contracted the virus early in the pandemic. This risk was observed in individuals with and without pre-existing heart conditions and confirms earlier research linking COVID-19 infection to a higher chance of cardiovascular events. However, this study is the first to indicate that the heightened risk may last as long as three years, especially for those infected during the first wave of the pandemic.

The study, published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, revealed that individuals who had COVID-19 early in the pandemic were twice as likely to experience cardiovascular events compared to those with no history of infection. For those with severe cases, the risk was nearly quadrupled.

“This study sheds new light on the potential long-term cardiovascular effects of COVID-19, a still-looming public health threat,” said David Goff, M.D., Ph.D., director for the Division of Cardiovascular Sciences at NIH’s National Heart, Lung, and Blood Institute (NHLBI), which largely funded the study. “These results, especially if confirmed by longer term follow-up, support efforts to identify effective heart disease prevention strategies for patients who’ve had severe COVID-19. But more studies are needed to demonstrate effectiveness.”


Genetic Factors and Blood Type’s Role in COVID-19 Complications

The study is also the first to show that an increased risk of heart attack and stroke in patients with severe COVID-19 may have a genetic component involving blood type. Researchers found that hospitalization for COVID-19 more than doubled the risk of heart attack or stroke among patients with A, B, or AB blood types, but not in patients with O types, which seemed to be associated with a lower risk of severe COVID-19.

Scientists studied data from 10,000 people enrolled in the UK Biobank, a large biomedical database of European patients. Patients were ages 40 to 69 at the time of enrollment and included 8,000 who had tested positive for the COVID-19 virus and 2,000 who were hospitalized with severe COVID-19 between Feb. 1, 2020, and Dec. 31, 2020. None of the patients had been vaccinated, as vaccines were not available during that period.

The researchers compared the two COVID-19 subgroups to a group of nearly 218,000 people who did not have the condition. They then tracked the patients from the time of their COVID-19 diagnosis until the development of either heart attack, stroke, or death, up to nearly three years.


Higher Cardiovascular Risk in Patients With Severe Cases

Accounting for patients who had pre-existing heart disease – about 11% in both groups – the researchers found that the risk of heart attack, stroke, and death was twice as high among all the COVID-19 patients and four times as high among those who had severe cases that required hospitalization, compared to those who had never been infected. The data further show that, within each of the three follow-up years, the risk of having a major cardiovascular event was still significantly elevated compared to the controls – in some cases, the researchers said, almost as high or even higher than having a known cardiovascular risk factor, such as Type 2 diabetes.

“Given that more than 1 billion people worldwide have already experienced COVID-19 infection, the implications for global heart health are significant,” said study leader Hooman Allayee, Ph.D., a professor of population and public health sciences at the University of Southern California Keck School of Medicine in Los Angeles. “The question now is whether or not severe COVID-19 should be considered another risk factor for cardiovascular disease, much like type 2 diabetes or peripheral artery disease, where treatment focused on cardiovascular disease prevention may be valuable.”

Allayee notes that the findings apply mainly to people who were infected early in the pandemic. It is unclear whether the risk of cardiovascular disease is persistent or may be persistent for people who have had severe COVID-19 more recently (from 2021 to the present).


Need for Broader Studies and Vaccine Impact on Risks


Scientists state that the study was limited due to the inclusion of patients from only the UK Biobank, a group that is mostly white. Whether the results will differ in a population with more racial and ethnic diversity is unclear and awaits further study. As the study participants were unvaccinated, future studies will be needed to determine whether vaccines influence cardiovascular risk. Studies on the connection between blood type and COVID-19 infection are also needed as the mechanism for the gene-virus interaction remains unclear.

For more on this research:

How COVID Continues to Threaten Your Heart Years After Infection

COVID-19 Doubles Risk of Heart Attacks, Strokes, and Death

Reference: “COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type” by James R. Hilser, Neal J. Spencer, Kimia Afshari, Frank D. Gilliland, Howard Hu, Arjun Deb, Aldons J. Lusis, W.H. Wilson Tang, Jaana A. Hartiala, Stanley L. Hazen and Hooman Allayee, 9 October 2024, Arteriosclerosis, Thrombosis, and Vascular Biology.
DOI: 10.1161/ATVBAHA.124.321001

This study was supported by NIH grants R01HL148110, R01HL168493, U54HL170326, R01DK132735, P01HL147823, R01HL147883, and P30ES007048.
 

Zoner

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This is on Geert's page and not behind a paywall so he must want it read and passed around. Geert is generally pro-vaxxed so it's not surprising that he would write something like this. Maybe disappointing in some ways, although there are some vaccines that did work and did save lives so it's not a black and white, all or none situation. I think RFK would agree, he has repeatedly said he's not anti-vaxx, he just wants to make sure they work and are safe. Don't we all?


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My message to RFK Jr.: Think carefully before acting on your new vaccine policy.
Geert Vanden Bossche
Nov 08, 2024

The outcome of the U.S. election, with RFK Jr. overseeing public health issues, will bring about a spectacular shift in public health policy. This is a welcome change, as the incompetence, conflicts of interest, and stubbornness of health authorities in the U.S. and beyond are disheartening. However, as a vaccinologist, I am somewhat concerned about the extreme polarization that America is currently experiencing. This polarization now threatens to penetrate even the deepest layers of society, including public health.

For every point of disagreement, the response nowadays seems to need to be black or white. These days, one is either an unconditional advocate of unrestricted vaccination practices or despises every needle that fits on a vaccine syringe. The scientific weighing of pros and cons—depending on the target group, type of vaccine, epidemiological situation, and objective data from relevant studies—seems to no longer be part of the decision-making process for many.

Often, arguments regarding the isolated impact on the individual are overly simplistic. I don’t mean to suggest that we, as a society, should just have to accept that our healthy children—who may never even become exposed to the disease they are being vaccinated against—being injected with substances that could potentially cause serious health issues, even if the latter would only occur on very rare occasions. Rather, I am referring to the general lack of awareness that so-called vaccine-preventable infectious diseases can only be contained through a form of immunity collectively mounted by the population, namely, herd immunity. This has become a topic that neither the so-called pro- nor anti-vaxxers wish to debate, likely because few truly understand its biological implications. I recently pointed out some common misunderstandings regarding this issue:


Herd immunity ensures that the spread of the virus is suppressed to the point where it no longer causes productive infections in individuals who lack protective immunity to the virus. Herd immunity can only be achieved when a large enough portion of the population builds an immune response that protects against productive infection. Such immunity develops spontaneously when, for example, a population is overwhelmed by a pandemic caused by a virus that naturally provokes an acute, self-limiting infection. Such viral infections (e.g., SARS-CoV-2) can spread rapidly through asymptomatic shedding but are usually quickly contained by cytotoxic immune effector cells in individuals who develop symptomatic infection (hence, the self-limiting nature of these infections).

Symptomatically infected individuals are protected from productive infection upon subsequent exposure, thanks to trained innate immunity, which may be combined with a recall of previously induced, virus-neutralizing antibodies (Abs). Consequently, larger portions of the population will eventually have sterilizing immunity after natural infection. In many cases, especially among children and young healthy people, a well-trained first line of immune defense as the sole natural immune response suffices to prevent productive infection upon exposure. This already explains why in a young and healthy population, the level of herd immunity cannot be assessed by measuring the increase in serum titers of (neutralizing) Abs. Such measurement of so-called seroconversion in the population would lead to a serious underestimation of herd immunity. Conversely, when virus spread is controlled by herd immunity, innate immunity will weaken, and neutralizing Ab concentrations in the blood will decrease, reducing herd immunity. This, however, is not a problem as long as the population is not exposed to an external source of the virus, or a sufficient portion of the population possesses an immunological memory of neutralizing Abs. However, individuals who have not previously contracted the disease or didn’t even get infected at all are at risk of becoming ill, or even severely ill, when herd immunity wanes. This is why and how maintaining herd immunity can prevent recurrent epidemics.

Immunizing the immunologically naive portion of the population (e.g., newborns) with live-attenuated vaccines not only strengthens innate immunity but also establishes an immunological memory of adaptive Abs, thereby contributing both to the individual protection of the vaccinated and to maintaining herd immunity in the population. While maintaining herd immunity can prevent recurrent epidemics, it cannot prevent a pandemic caused by a highly divergent viral variant due to the specificity of the Abs produced by previously infection- or vaccine-induced memory B cells. It is therefore not surprising that these live-attenuated vaccines can only be used to prevent epidemics caused by specific viruses that not only provoke acute, self-limiting infections but also have a high degree of genetic stability (e.g., measles, mumps, rubella virus).

I therefore continue to advocate for a new vaccine approach that enables training of broad, non-variant-specific cell-mediated innate immunity to prevent productive infection through sterilizing immunity. Such an immune intervention would not only protect the vaccinated individual from illness but also protect immunologically naive individuals by sufficiently curbing virus transmission within the population to prevent productive infection in these individuals.

I therefore continue to argue that a laissez-faire attitude toward viruses capable of rapidly spreading through entire populations and causing acute, potentially fatal infections is a flawed approach, as it will create gaps in the population's herd immunity. Even in industrialized countries, good general and personal hygiene and adequate sanitary conditions cannot guarantee protection against these viruses, especially when they are also airborne. Large gaps in herd immunity can quickly lead to high infection pressure, where it is even conceivable that the virus could cause severe breakthrough infections in immunologically primed individuals.

There are indeed approaches with the potential to enhance natural, cell-based innate immunity (e.g., Natural Killer cell vaccines) in a way that provides broad protection against a multitude of respiratory viruses and other infectious agents (or even non-infectious agents like allergens). However, it goes without saying that the vaccine industry is not interested in developing such broad-spectrum vaccines as deploying immune interventions that can prevent or treat multiple diseases/infections simultaneously does not represent a lucrative objective. On the other hand, the notion that we should throw out the baby with the bathwater and focus solely on personalized vaccinology, even for infectious diseases that manifest at a population level, is at best short-sighted.
Evidently RFK Jr. does not agree. He sued Fauci for calling him a liar that the 72 Vaccines on a schedule for children have never been tested.

video 2:43 runtime
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1 in 5 people could have long COVID
by Dennis Thompson
November 10, 2024

More than 1 in 5 Americans likely suffer from long COVID, a new AI-assisted review has found.

The analysis suggests that nearly 23% of U.S. adults experience the symptoms of long COVID, according to results published Nov. 8 in the journal Med.

That's much higher than the 7% prevalence of long COVID that's been suggested by other studies, researchers said.

"Questions about the true burden of long COVID -- questions that have thus far remained elusive -- now seem more within reach," said senior researcher Hossein Estiri, head of AI research at Mass General Brigham in Boston.

For the study, researchers developed an AI tool that can sift through mounds of electronic health records looking for the frequently subtle symptoms related to long COVID.

These symptoms can occur in a wide range of body systems, and include fatigue, chronic cough, heart problems and "brain fog." They typically develop weeks or months after a person shakes off their initial COVID-19 infection.

"Our AI tool could turn a foggy diagnostic process into something sharp and focused, giving clinicians the power to make sense of a challenging condition," Estiri said in a Mass General news release.

The AI specifically looks for symptoms that can't be explained by a person's medical history, have persisted for two months or longer and occur following a COVID infection, researchers said.

For example, the AI can detect if shortness of breath might be explained by pre-existing heart failure or asthma, rather than long COVID.

"Physicians are often faced with having to wade through a tangled web of symptoms and medical histories, unsure of which threads to pull, while balancing busy caseloads. Having a tool powered by AI that can methodically do it for them could be a game-changer," said lead researcher Dr. Alaleh Azhir, an internal medicine resident at Brigham and Women's.

Based on these parameters, the AI estimated that nearly 23% of Americans likely have long COVID, a figure that researchers argue aligns more closely with national trends.

The researchers plan to release the AI publicly on open access, so doctors and health care systems can employ and test it.

More information: Precision Phenotyping for Curating Research Cohorts of Patients with Unexplained Post-Acute Sequelae of COVID-19, Med (2024). DOI: 10.1016/j.medj.2024.10.009. www.cell.com/med/fulltext/S2666-6340(24)00407-0
 

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It often takes scientists an incredibly long time to understand things that are pretty obvious with simple common sense...
Geert Vanden Bossche
Nov 12, 2024


“Our findings suggest that vaccine plays an important role in the evolution of the virus genome”…”These mutations become fixed in the viral population due to the selective pressure imposed by vaccination.”

Geert:
Tjiens, was daar ooit geen soort van Vlaamse plattelandsveearts die precies hiervoor waarschuwde maar belachelijk werd gemaakt door Knack?

Translation: Huh, wasn’t there some kind of Flemish country vet who warned about this exact thing but was ridiculed by Knack?

(Inloggen : "How anti-vaxxers made a Flemish veterinarian world-famous")
 

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Latest updates show that a new SARS-CoV-2 variant called MV.1 is likely to be the next contender to XEC variant
Nikhil Prasad Fact checked by:Thailand Medical News Team
Nov 12, 2024

The global landscape of SARS-CoV-2 variants continues to evolve, with the latest updates suggesting that a new SARS-CoV-2 variant called MV.1 may soon pose a significant challenge to the current dominant XEC variant.


First identified in Maharashtra, India, MV.1 appears to be rapidly gaining ground worldwide, raising questions about its potential impact on future COVID-19 waves. Researchers are closely monitoring MV.1’s growth patterns and mutations, which may give it an edge over other emerging lineages, particularly in North America and parts of Asia.


MV.1’s Global Emergence and Characteristics
MV.1 originated in India in June 2024, evolving from the JN.1.49 lineage through MB.1.1.1. The variant’s mutations, including a reversion of the Spike K478T mutation to its ancestral Wuhan form, may be contributing to its growing prevalence. Initially, MV.1 was confined mainly to India; however, recent samples indicate its spread across various locations, including the United States, Mauritius, Singapore, and Australia.

Wastewater surveillance has proven valuable in tracking MV.1’s spread. In just the past two weeks, MV.1 has appeared in multiple U.S. states such as Kansas, Michigan, Massachusetts, Florida, Pennsylvania, Delaware, and New York.

Notably, MV.1 was found to be the dominant variant in Muskegon County, Michigan, and Miami, Florida, suggesting its potential to outcompete other variants in specific locales. In addition, data from Sullivan County, New Hampshire, shows MV.1 dominating wastewater samples in the region. However, out of 500 samples, it was not as widely prevalent, indicating that it may be in the early stages of establishment.


x.com


Comparative Growth of MV.1 vs. XEC and Other Contenders
MV.1’s competitive growth advantage has captured the attention of researchers. Globally, it shows a 4.4% growth rate per day, equivalent to about a 31% increase weekly against the JN.1. and DeFLuQE variants, the latter of which encompasses the KP.3.1.1 lineage. Although MV.1's growth is slightly slower than XEC's, it has nevertheless demonstrated a consistent upward trend in areas where it has gained a foothold.

The XEC variant, currently dominant in many regions, exhibits a growth advantage of around 4.9% per day globally. Given XEC’s rapid spread and dominance, it would take a strong contender to challenge its place, with LP.8.1 and MC .10.2 also among potential rivals besides MV.1


x.com

LP.8.1 has gained attention for its success in parts of Asia and the United States, showing a 6% daily growth advantage over XEC. MC.10.2, with an 11.1% daily growth advantage, is emerging rapidly in Canada and New Zealand, suggesting a potential crossover with XEC in late November. Despite these contenders, MV.1’s rising presence across multiple continents may make it one of the most likely successors to XEC.

However, Thailand Medical News would like to warn readers that the SARS-CoV-2 variant issues are extremely dynamic as the various variants in circulation are rapidly spawning newer sub-lineages or are recombining with different variants to produce newer strains and sub-lineages with vary viral fitness and chracteristics. Hence newer viral strain contenders for predominance can emerge at any time.


Key Mutations and Potential Implications

MV.1’s evolution includes notable mutations that could influence its transmissibility and immune evasion. The reversion of the K478T mutation to its ancestral form, along with the presence of other mutations such as 346T, 456V, 478T, 493Q are key aspects that researchers believe may impact the virus’s behavior. These genetic changes distinguish MV.1 from previous lineages, potentially providing it with unique advantages over other SARS-CoV-2 variants.

The S:F456V, mutation, commonly found in cryptic lineages, had rarely been observed in circulation until now. With MV.1 containing this mutation, scientists are paying close attention to its transmission dynamics and its ability to evade immunity, particularly in vaccinated populations. Since MV.1 also harbors a reversion in the S:478 back to T - adjacent to the 456V mutation - it allows researchers to screen for it with a high degree of accuracy, especially in regions with comprehensive wastewater surveillance.


Global Implications and the Future of SARS-CoV-2 Variants
The emergence of MV.1 raises broader questions about the future trajectory of COVID-19. With several contenders - including LP.8.1, MC.10.2, and XEC.4 - all showing varying levels of growth advantage, predicting the next dominant strain remains challenging. However, MV.1’s unique genetic profile, combined with its relatively fast spread, may position it as one of the stronger candidates for dominance, especially as it continues to gain ground in underserved and undersampled regions.

Researchers emphasize the importance of continuous monitoring, as the ongoing adaptation of SARS-CoV-2 underscores the virus’s capacity for rapid evolution. Wastewater surveillance, in particular, will play an increasingly vital role in identifying emerging variants and providing timely data on their spread, especially as clinical testing decreases in frequency worldwide.


Conclusion: MV.1 as a Potential Game-Changer
As the battle for SARS-CoV-2 dominance intensifies, MV.1 stands out as a variant with significant potential. Its growth patterns, genetic mutations, and success in previously low-prevalence regions indicate that it could soon become a major player in the global COVID-19 landscape. While other variants like LP.8.1 and MC.10.2 are also showing strong growth, MV.1’s rapid spread across multiple continents suggests it may have the staying power needed to challenge XEC’s current dominance.

Continued research and monitoring are essential as scientists work to understand the implications of MV.1’s unique mutations and growth patterns. With the possibility of a new variant-driven wave on the horizon, staying informed and prepared is more crucial than ever.
 

Heliobas Disciple

TB Fanatic
View: https://www.youtube.com/watch?v=jndykWR9O-c
Excess deaths published
Dr. John Campbell
Nov 13, 2024
19 min 22 sec

Excess mortality across countries in the Western World since the COVID-19 pandemic: ‘Our World in Data’ estimates of January 2020 to December 2022 https://bmjpublichealth.bmj.com/conte... Our world in data https://ourworldindata.org/grapher/ex... Human Mortality Database (2024); World Mortality Dataset (2024); Karlinsky and Kobak (2021); Human Mortality Database (2024); World Mortality Database (2024) – processed by Our World in Data https://ourworldindata.org/excess-mor... Introduction Excess mortality during the COVID-19 pandemic has been substantial, includes not only deaths from SARS-CoV-2 infection but also deaths related to the indirect effects of the health strategies Insight into excess death rates in years following WHO’s pandemic declaration is crucial for government leaders and policymakers to evaluate their health crisis policies. This study explores excess mortality in the Western World from 2020 until 2022. Although COVID-19 vaccines were provided to guard civilians from suffering morbidity and mortality by the COVID-19 virus, suspected adverse events have been documented as well Methods All-cause mortality reports were abstracted for countries using the ‘Our World in Data’ database. Excess mortality, deviation between the reported number of deaths in a country during a certain week or month, and the expected number of deaths in a country for that period under normal conditions. Karlinsky and Kobak (2021) This model uses historical death data in a country from 2015 until 2019 and accounts for seasonal variation and year-to-year trends in mortality. Results 1 January 2020 until 31 December 2022 The total number of excess deaths in 47 countries of the Western World was 3, 098, 456 Excess mortality was documented in: 41 countries (87%) in 2020 42 countries (89%) in 2021 43 countries (91%) in 2022. In 2020 (the year of the COVID-19 pandemic onset and implementation of containment measures) 1, 033, 122 excess deaths (P-score 11.4%) In 2021 (the year in which both containment measures and COVID-19 vaccines were used to address virus spread and infection) the highest number of excess deaths was reported: 1, 256, 942 excess deaths (P-score 13.8%) In 2022 (when most containment measures were lifted and COVID-19 vaccines were continued) 808, 392 excess deaths (P-score 8.8%). Conclusions Excess mortality has remained high in the Western World for three consecutive years, despite the implementation of containment measures and COVID-19 vaccines. This raises serious concerns. Government leaders and policymakers need to thoroughly investigate underlying causes of persistent excess mortality. More details Previous research confirmed profound under-reporting of adverse events, including deaths, after immunisation Consensus is also lacking in the medical community regarding concerns that mRNA vaccines might cause more harm than initially forecasted. French studies suggest that COVID-19 mRNA vaccines are gene therapy products requiring long-term stringent adverse events monitoring Although the desired immunisation through vaccination occurs in immune cells, some studies report a broad biodistribution and persistence of mRNA in many organs for weeks. Batch-dependent heterogeneity in the toxicity of mRNA vaccines was found in Denmark. Simultaneous onset of excess mortality and COVID-19 vaccination in Germany provides a safety signal warranting further investigation. Despite these concerns, clinical trial data required to further investigate these associations are not shared with the public. Autopsies to confirm actual death causes are seldom done. Governments may be unable to release their death data with detailed stratification by cause, although this information could help indicate whether COVID-19 infection, indirect effects of containment measures, COVID-19 vaccines or other overlooked factors play an underpinning role. Expression of concern https://bmjpublichealth.bmj.com/conte... Other work by Saskia Mostert https://www.researchgate.net/scientif... Other work by Gertjan Kaspers https://researchinformation.amsterdam...
 
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