marsh
On TB every waking moment
51:19 min
Ivanka Trump Discusses Find Something New: A Campaign to Promote Multiple Career Pathways
•Streamed live 5 hours ago
The White House
CORONA Main Coronavirus thread
- Thread starter Heliobas Disciple
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51:19 min
Ivanka Trump Discusses Find Something New: A Campaign to Promote Multiple Career Pathways
•Streamed live 5 hours ago
The White House
marsh
On TB every waking moment
4:06 min
Demonstration of Donning (Putting On) Personal Protective Equipment (PPE)
•Jul 14, 2020
Centers for Disease Control and Prevention (CDC)
This video is intended for healthcare personnel (HCP) caring for patients with suspected or confirmed COVID-19. It demonstrates one method described in CDC’s infection control guidance for donning (putting on) personal protective equipment (PPE) in healthcare settings.
marsh
On TB every waking moment
11:24 min
NOT A COINCIDENCE: Federal debt, COVID lockdowns, BLM protests & CAIR are all connected
•Jul 14, 2020
Glenn Beck
Every American should start writing a diary, or preserving the hard copies of things -- artifacts, news articles, objects bought from stores...because we ARE under attack. And incidences that may seem like isolated events (the skyrocketing federal debt, the loss of America's entrepreneurial spirit, COVID 19 lockdowns that destroy businesses, Black Lives Matter protests, and anti-Semitic movements) are not isolated at all. It's not a coincidence all these happened at once. And now, as seen in recent protests, BLM Marxists, anarchists, AND islamists (CAIR) are all working together. Our churches MUST wake up, because it's the only way we can fix this.
marsh
On TB every waking moment
38:00 min
Coronavirus Update With CDC Director, Robert R. Redfield, MD
•Streamed live 2 hours ago
JAMA Network
CDC Director Robert R. Redfield, MD discusses the ongoing COVID-19 pandemic and the agency’s latest recommendations. Recorded on July 14, 2020.
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LIVE
Multiplicity of Randomized Clinical Trials for Coronavirus Disease 2019
JAMA NetworkJuly 14, 2020
Ramez Kouzy, MD, Joseph Abi Jaoude, MD, and Ethan Ludmir, MD join JAMA Network Open Digital Media Editor, Seth Trueger, MD, MPH, to discuss a systematic review that finds multiplicity of trials for #COVID19 offers replication & validation, but carries high risk of false positivity and competition for participants. Read the article here: Characteristics of the Randomized Clinical Trials for COVID-19 Launched During the Pandemic.
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marsh
On TB every waking moment
4:54 min
California closes back down as COVID-19 cases rise l ABC News
•Jul 14, 2020
ABC News
Los Angeles schools, the second biggest school district in the country, will not return to in-person learning in August.
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7:13 min
Florida among 12 states seeing record COVID-19 cases, many traced to large gatherings
•Jul 13, 2020
ABC News
Florida saw the highest single-day total of new cases out of any state since the pandemic began -- over 15,000. In Miami, neighbors have expressed concerns over parties at nearby residences.
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marsh
On TB every waking moment
LIVE
WATCH LIVE: Polis provides update on Colorado’s response to COVID-19
•Started streaming 29 minutes ago
9NEWS
WATCH LIVE AT 2 P.M.: Gov. Jared Polis provides an update on the state’s response to the COVID-19 pandemic amid surges of the virus in neighboring states.
marsh
On TB every waking moment
LIVE
LIVE: A Conversation With Dr. Anthony Fauci at Georgetown University
•Started streaming 22 minutes ago
Bloomberg QuickTake News
(July 14) Watch live as Dr. Anthony Fauci speaks to Institute of Politics and Public Service at Georgetown’s McCourt School of Public Policy and the Global Health Initiative on coronavirus. Fauci, the Director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health and a member of the White House Coronavirus Task Force, will join Georgetown students for an update on the COVID-19 pandemic, a consideration of its implications for public policy, and a candid conversation on the unique risks and responsibilities young people have in mitigating the spread of COVID-19. The inherent uncertainty of a global pandemic, combined with our evolving and changing understanding of the disease and the effectiveness of potential interventions, presents a unique challenge for policymakers. The situation is further complicated by the significant spread of misinformation and disinformation on social media, making it difficult to rally support around necessary policies. As one of the most visible leaders in public health, Dr. Fauci brings years of experience and deep expertise to global and national efforts to combat COVID-19.
marsh
On TB every waking moment
LIVE
LIVE: Vice President Mike Pence visits Louisiana amid coronavirus surge
•Started streaming 36 minutes ago
Yahoo Finance
Vice President Mike Pence visits Louisiana amid coronavirus surge.
marsh
On TB every waking moment
11:33 min
Coronavirus vaccine update: How close are we? | COVID-19 Special
•Jul 14, 2020
DW News Germany
As Covid-19 cases spike in some countries, it’s clear that the pandemic isn’t slowing down. That’s why many are pinning their hopes on a vaccine. Thousands of scientists are now working on more than 150 vaccines, but none have been approved for use. The US Food and Drug Administration has granted Fast Track designation to COVID-19 vaccine candidates under development by Pfizer and its German partner BioNTECH. So just how close are we to getting an effective coronavirus vaccine?
___________________________________________
5:46
California shuts down again as coronavirus cases surge | DW News
•Jul 14, 2020
DW News Germany
Amid an ongoing surge in coronavirus cases across several US states, California's governor Gavin Newsom has announced the state is once again shutting down. State authorities have ordered closures of restaurants, bars, gyms, shopping malls and churches across America's most populous state. Several rural counties are experiencing strains to their hospital systems, while cases are also mounting in large metropolitan areas including Los Angeles and San Francisco. DW's Stefan Simons reports on the coronavirus crisis in the USA.
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marsh
On TB every waking moment
LIVE (waiting)
President Trump Holds a Press Conference
•Started streaming 13 minutes ago
The White House
marsh
On TB every waking moment
4:39 min
California shuts down again as COVID-19 cases surge
•Jul 14, 2020
CBC News Canada
California rolls back on reopening as cases of the novel coronavirus climb. Restaurants, bars, malls, gyms, salons are being shut down again with the state now averaging more than 8,000 new cases a day.
marsh
On TB every waking moment
5:34 min
How the coronavirus spike is affecting Texas retail, restaurants
•Jul 14, 2020
CNBC Television
Ray Washburne, chairman and CEO of Charter Holdings, joins "Squawk Alley" to discuss the retail and restaurant business in Texas amid the coronavirus outbreak.
marsh
On TB every waking moment
2:38:57 min
Florida Governor Ron DeSantis gives a coronavirus update
•Streamed live 4 hours ago
Yahoo Finance
Florida Governor Ron DeSantis gives a coronavirus update.
marsh
On TB every waking moment
5:38 min
Stanford Medicine dean on the resurgence of coronavirus cases
•Jul 14, 2020
CNBC Television
Dr. Lloyd Minor, dean of Stanford Medicine, joins "Squawk on the Street" after his conversation with Dr. Anthony Fauci to discuss the spread of coronavirus in the U.S.
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4:28 min
Focus on economic data rather than virus headlines: Strategist
•Jul 14, 2020
CNBC Television
Falling tech stocks pulled the Nasdaq and S&P 500 lower in Monday's session, led by Netflix, Microsoft, Amazon and Facebook. Krishna Memani, former vice chairman of investments at Invesco, joins "Squawk Box" to discuss.
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marsh
On TB every waking moment
1:30 min
How Trump has undercut the CDC on coronavirus
•Jul 14, 2020
Washington Post
President Trump has undermined or contradicted guidance from the Centers for Disease Control and Prevention at least a half dozen times since the coronavirus outbreak began.
marsh
On TB every waking moment
8:05min
U.S. schools face pressure to reopen as coronavirus cases soar
•Jul 14, 2020
CBS News
Dr. Dyan Hes, a pediatrician in New York City, joined CBSN to discuss how important it is to have a clear, unified message from the Trump administration on how to safely get kids back in the classroom, plus a new study that suggests nearly 1.5 million teachers are at high risk of contracting a serious coronavirus infection.
marsh
On TB every waking moment
2:47 min
Coronavirus Surges Strain Testing Capacity Nationwide | TODAY
•Jul 14, 2020
TODAY
As coronavirus cases surge across the country, so has the demand for testing. The problem is that there are simply not enough resources to keep up. NBC’s Sam Brock reports for TODAY from Miami Beach, one of the country’s newest hot spots.
marsh
On TB every waking moment
10:06 min
Coronavirus: White House targets US disease chief Dr Anthony Fauci - BBC News
•Jul 14, 2020
BBC News
US infectious disease chief Dr Anthony Fauci is being targeted by the Trump administration as tensions rise between the health expert and the president.
marsh
On TB every waking moment
6:34 min
McEnany downplays fears of reopening schools
•Jul 14, 2020
Fox News
White House Press Secretary Kayleigh McEnany discusses push to reopen schools with Harris Faulkner on 'Outnumbered Overtime.'
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8:47 min
Sen Rubio explains who will be hit hardest if schools don't reopen
•Jul 14, 2020
Fox News
Republican Sen. Marco Rubio warns working and low-income families will be hurt the most the longer schools stay closed.
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4:45 min
Military medical personnel deploy to Texas to aid in COVID-19 response
•Jul 14, 2020
Fox News
Dr. Natasha Kathuria shares the real story about what's happening at Texas hospitals as military medical personnel deploy to the state.
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marsh
On TB every waking moment
We Are Slowly but Steadily Unraveling the Genetics of This Pandemic | National Review
Genes are likely to play a factor in which antibodies are most effective against the virus, as well as in who can fight off the virus easily.
www.nationalreview.com
We Are Slowly but Steadily Unraveling the Genetics of This Pandemic
By JIM GERAGHTY
July 13, 2020 1:56 PM
Today, a team led by scientists at Scripps Research announced they had discovered a common feature found in many of the human antibodies that neutralize SARS-CoV-2:
Genes are likely to play a factor in which antibodies are most effective against the virus, just as genes probably play a factor in who can fight off the virus easily and who succumb to it rapidly.
You probably heard about the New Jersey family that lost four members in rapid succession, including one who had no discernable previous health issues, or the elderly Louisiana woman and her three sons all dying within a week or so, or the three members of a family dying in rapid succession in Florida. Genetics were probably not the only reason these families were struck so severely, but if one parent had genes that made them particularly vulnerable to this particular strain of SARS-CoV-2, they may have passed along those genes to their children.
Yet there are people more than 100 years old — sometimes overweight or obese, smokers, and non-exercisers who catch the virus and manage to pull through. They’re blessed with genetics that makes their immune systems and white blood cells work effectively, even if their health is not ideal otherwise.
At the beginning of June, teams of medical researchers in Germany, Spain, and Italy found “variations at two spots in the human genome are associated with an increased risk of respiratory failure in patients with Covid-19. . . . One of these spots includes the gene that determines blood types. Having Type A blood was linked to a 50 percent increase in the likelihood that a patient would need to get oxygen or to go on a ventilator.”
The other spot on the genome is six genes on Chromosome 3; earlier this month, additional research determined that this stretch of DNA was passed along from Neanderthals 60,000 years ago. The thinking is, the more this particular gene or genes are in a person’s genetic code, the more vulnerable they are to SARS-CoV-2.
13
From a layman’s perspective, genetics is weird and pretty darn unfair; science has determined that some small populations of human beings have near-immunity to anthrax and malaria. Some people might be unnerved at this sort of research, looking for connections between genes and vulnerability to diseases, as it could feed into notions that some people are genetically “superior,” and represent a step down the road to eugenics. But recognizing the reality of genetic differences does not inherently require one to think of other human beings as “lesser” in any way. Look hard enough at anybody’s genome and you’ll probably find some gene that puts them at a disadvantage in one circumstance or another.
If we’re going to beat this virus, we have to understand it as thoroughly as possible — including clues as to who might be more vulnerable to it and why.
NOW WATCH: 'New Flu Virus Found In Pigs In China Has Pandemic Potential' .38 min
danielboon
TB Fanatic
Massachusetts Coronavirus: 8,125 deaths, 105,986 total confirmed cases Massachusetts Coronavirus: 8,125 deaths, 105,986 total confirmed cases 10 new deaths up from yesterday 203 new cases up from yesterday
Indiana
I wish the politicians would make sure their areas have sufficient supplies of masks before they make them mandatory. Some of the stores in Plainfield got wiped out of masks; likely by the Indy folks who couldn't find them there.
Mask order goes into effect in West Lafayette to help stop spread of coronavirus
Posted: Jul 14, 2020 / 09:26 AM EDT / Updated: Jul 14, 2020 / 09:26 AM EDT
WEST LAFAYETTE, Ind. – Right now, four Indiana counties—including Marion County—require face masks in an effort to slow the spread of the coronavirus.
On Monday, the City of West Lafayette joined them when Mayor John Dennis signed an emergency order requiring masks.
Face coverings must be worn in businesses that are open to the public, on all forms of public transportation, crowded work settings, and any outdoor space where someone can’t maintain social distancing.
Evansville is also considering requiring face masks soon.
fox59.com
I wish the politicians would make sure their areas have sufficient supplies of masks before they make them mandatory. Some of the stores in Plainfield got wiped out of masks; likely by the Indy folks who couldn't find them there.
Mask order goes into effect in West Lafayette to help stop spread of coronavirus
Posted: Jul 14, 2020 / 09:26 AM EDT / Updated: Jul 14, 2020 / 09:26 AM EDT
WEST LAFAYETTE, Ind. – Right now, four Indiana counties—including Marion County—require face masks in an effort to slow the spread of the coronavirus.
On Monday, the City of West Lafayette joined them when Mayor John Dennis signed an emergency order requiring masks.
Face coverings must be worn in businesses that are open to the public, on all forms of public transportation, crowded work settings, and any outdoor space where someone can’t maintain social distancing.
Evansville is also considering requiring face masks soon.
Mask order goes into effect in West Lafayette to help stop spread of coronavirus
WEST LAFAYETTE, Ind. – Right now, four Indiana counties—including Marion County—require face masks in an effort to slow the spread of the coronavirus. On Monday, the City of West Lafayette joined t…
fox59.com
I just happened across the Federal Bureau of Prisons' dashboard; it includes an interactive map of all the federal prisons. Some states don't have any.
07/13/2020 - The BOP has 129,927 federal inmates in BOP-managed institutions and 13,634 in community-based facilities. The BOP staff complement is approximately 36,000. There are 3,112 federal inmates and 259 BOP staff who have confirmed positive test results for COVID-19 nationwide. Currently, 5,141 inmates and 615 staff have recovered. There have been 95 federal inmate deaths and 1 BOP staff member death attributed to COVID-19 disease.
www.bop.gov
07/13/2020 - The BOP has 129,927 federal inmates in BOP-managed institutions and 13,634 in community-based facilities. The BOP staff complement is approximately 36,000. There are 3,112 federal inmates and 259 BOP staff who have confirmed positive test results for COVID-19 nationwide. Currently, 5,141 inmates and 615 staff have recovered. There have been 95 federal inmate deaths and 1 BOP staff member death attributed to COVID-19 disease.
BOP: COVID-19 Update
www.bop.gov
The worker at Meijer told me today her friend made the mask she was wearing. She pointed out the ear loops were made from T-shirt material because there is no elastic to be had easily. With this in mind, it might be a good idea to keep the ear loops and that little piece of metal noseband from the masks you throw away.
Provisional Death Counts for Coronavirus Disease 2019 (COVID-19)
National Center for Health Statistics
jward
passin' thru
Reuters
@Reuters
3m
U.S. CDC head says mask-wearing could get COVID-19 under control within 4-8 weeks https://reut.rs/2C2wc31
View: https://twitter.com/Reuters/status/1283220998385479680?s=20
@Reuters
3m
U.S. CDC head says mask-wearing could get COVID-19 under control within 4-8 weeks https://reut.rs/2C2wc31
View: https://twitter.com/Reuters/status/1283220998385479680?s=20
PanBear
Veteran Member
Agreement (Covid-19) Form
This is how terrified @GavinNewsom has made local salons in CA.. You have to SIGN A PERMISSION SLIP for service!!!! WHAT?!?! Now salons are asking health related questions?? What’s next?? Prove of a vaccine??? #COVID
View: https://twitter.com/CMF32575604/status/1282859073453428736
This is how terrified @GavinNewsom has made local salons in CA.. You have to SIGN A PERMISSION SLIP for service!!!! WHAT?!?! Now salons are asking health related questions?? What’s next?? Prove of a vaccine??? #COVID
View: https://twitter.com/CMF32575604/status/1282859073453428736
PanBear
Veteran Member
Covid-19 death count will not change.
How many other states are counting alternate causes of death as COVID deaths?
This is why the data is flawed.
#Illinois
video 1:56 min
View: https://twitter.com/Sammicordova/status/1282364528882094080
How many other states are counting alternate causes of death as COVID deaths?
This is why the data is flawed.
#Illinois
video 1:56 min
View: https://twitter.com/Sammicordova/status/1282364528882094080
marsh
On TB every waking moment
41:29 min
Man, Covid-19 Just Keeps Getting Worse...
•Premiered 5 hours ago
Peak Prosperity
Sick and tired of this pandemic yet? We sure are. But sadly, covid-19 increasingly looks like it's going to be with us for a LONG time to come.
Globally, cases are mounting fast, with the time it takes to hit the next million infected shorter than ever. And not only are we learning people can contract the virus a second time, it's looking like a meaningful number of patients can get it even more times than that. And successive infections appear to have symptoms that are every bit as intense as the first. Even among those who 'recover' -- even those cases that were asymptomatic -- numerous patients display long term organ damage (heart, lungs, kidneys, etc).
Chris walks through the latest findings on each of these worrisome topics, yet also shares the more optimistic data indicating the cheap and widely-available drug Ivermectin makes any important positive difference in reducing the damage covid-19 inflicts.
_____ LINKS FROM THIS VIDEO: Lasting Heart Damage https://www.newsweek.com/scans-reveal... Heart Study results https://academic.oup.com/ehjcimaging/... My Patient caught Covid twice https://www.vox.com/2020/7/12/2132165... Family caught it twice https://www.reddit.com/r/COVID19posit... Likely reinfected https://www.reddit.com/r/COVID19posit... Asymptomatic doesn’t mean healthy https://www.newsweek.com/coronavirus-... Ivermectin US trial http://www.pharmafile.com/news/550818... Ivermectin Works! https://www.trialsitenews.com/ivermec... Ivermectin Works! https://www.medrxiv.org/content/10.11... Antibodies don’t last – no herd immunity? https://www.businessinsider.com/coron...
https://www.youtube.com/watch?v=K4SQ-NOV-iU
marsh
On TB every waking moment
Toxicol Rep. 2020; 7: 658–663.
Published online 2020 Apr 30. doi: 10.1016/j.toxrep.2020.04.012
PMCID: PMC7192087
PMID: 32355638
Editorial: Nicotine and SARS-CoV-2: COVID-19 may be a disease of the nicotinic cholinergic system
Konstantinos Farsalinosa,b,*
aLaboratory of Mol. Biology and Immunology, Department of Pharmacy, University of Patras, Panepistimiopolis, 26500, Greece
bSchool of Public Health, Department of Public and Community Health, University of West Attica, 11521, Greece
Raymond Niaura
Departments of Social and Behavioral Science and Epidemiology, College of Global Public Health, New York University, USA
Jacques Le Houezec
Laboratory of Mol. Biology and Immunology, Department of Pharmacy, University of Patras, Panepistimiopolis, 26500, Greece
Anastasia Barbouni
School of Public Health, Department of Public and Community Health, University of West Attica, 11521, Greece
Aristidis Tsatsakis
Department Medicine, University of Crete, Greece
Dimitrios Kouretas
Department of Biochemistry and Biotechnology, University of Thessaly, Larisa, 41500, Greece
Apostolos Vantarakis
School of Medicine, University of Patras, Panepistimiopolis, 26500, Greece
Konstantinos Poulas
Laboratory of Mol. Biology and Immunology, Department of Pharmacy, University of Patras, Panepistimiopolis, 26500, Greece
Author information Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
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1. Introduction
As of 20 April, almost 1.7 million people globally have been diagnosed with Corona Virus Disease 2019 (COVID-19), a pandemic that has evolved from the emergence of a new coronavirus strain, acute respiratory syndrome coronavirus 2 (SARS-CoV-2), in China. More than 170,000 deaths have been reported, while there are certainly many more cases of milder disease that have not been diagnosed and officially confirmed due to limited testing capacity in most countries. The pandemic is a global emergency due to the rapid transmission of the disease and the potential to overwhelm the healthcare systems, and is expected to have considerable economic and health impacts. Contributing factors and their possible role in the relatively high infection, death rates between countries and origin have recently been studied [1,2]. This new outbreak has been additionally evaluated for current knowledge on coronaviruses based on a short history to epidemiology, pathogenesis, clinical manifestation of the disease, as well as treatment and prevention strategies [3]. The search for potential protective and therapeutic antiviral strategies is of particular and urgent concern [4].
While in most cases, especially in young people without any comorbidities, the disease is expected to be relatively mild, there is a substantial proportion of patients who develop complications and need intensive care-unit support and mechanical ventilation. In one case series of 1099 patients in China [5], 6.1 % of cases suffered from the primary composite end-point of admission to an intensive care unit, use of mechanical ventilation, or death. Patients with severe disease typically present with dyspnea and hypoxemia shortly after disease initiation, and may quickly progress to respiratory failure, acute respiratory distress syndrome (ARDS) and multi-organ failure [6]. Predictors of adverse outcomes include elevated levels of inflammatory markers and pro-inflammatory cytokines. A study of 150 COVID-19 cases reported that elevated levels of C-reactive protein (CRP), ferritin and IL-6 were associated with death [7]. IL-6, an important pro-inflammatory cytokine, was elevated in fatal cases of COVID-19 in another study of 191 patients [8]. Another study of 452 patients reported that those with severe disease showed lymphocytopenia, neutrophilia, low levels of monocytes, eosinophils and basophils, and elevated levels of infection-related biomarkers and inflammatory cytokines [9]. Pathological examination of a case in China revealed bilateral diffuse alveolar damage, desquamation of pneumocytes, hyaline membrane formation and interstitial mononuclear inflammatory infiltrates [10]. Flow cytometry of peripheral blood revealed reduced levels of CD4+ and CD8 + T cells, which however were hyper-activated, and elevated concentration of pro-inflammatory CCR6+ Th17 in CD4 + T cells. Such findings are hallmarks of ARDS and resemble features observed in SARS and Middle Eastern Respiratory Syndrome [11,12]. Systemic vasculitis was also observed [10]. Therefore, it seems that immune dysregulation may be implicated in the pathophysiology of severe COVID-19.
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2. Cytokine storm
While for decades common thinking suggested that every immune response to antigenic invasion was always beneficial in averting potential damage, studies in the 1980s identified that immune cells produce proteins with pleiotropic properties, having the potential to be either beneficial or harmful [13]. The proteins, called cytokines, were found to cause clinical manifestations similar to sepsis such as hemodynamic instability, fever, and localized inflammation [14,15]. Cytokines are important in mediating both immune cell recruitment and complex intracellular signaling control mechanisms that characterize inflammation and infection control. They are expressed by numerous cells, including macrophages, monocytes, B cells and T cells, promote differentiation of T-helper cells and stimulate CD4+ cells [16]. While activation of the immune system is important in fighting pathogens, dysregulation of cytokine production may lead to uncontrolled effects that can ultimately be detrimental to health [16,17].
Cytokine storm (also called macrophage activation syndrome) is a systemic inflammatory response that can be triggered by a variety of factors such as infections and drugs [18]. It represents a failure of the inflammatory response to return to homeostasis. The resulting unregulated immune activity can potentially lead to catastrophic tissue damage. The term first appeared in 1993 in an article relevant to graft-versus-host disease [19]. Subsequently, cytokine storm was a phenomenon recognized in both viral and bacterial infections. It has been particularly studied in viral infections such as cytomegalovirus pneumonitis, influenza virus and SARS-CoV [[20], [21], [22], [23]]. Bermejo-Martin et al. [21] recruited both inpatients and outpatients during the first wave of the pandemic flu in 2009 (nvH1N1) and examined the effects of immune host responses to the evolution of mild or severe disease by measuring serum levels of several chemokines and cytokines. They found a dramatic increase of mediators that stimulate Th-1 and Th-17 responses (which are responsible for attacking intracellular pathogens and clearing pathogens during host defence reactions) among severe hospitalized patients compared to milder cases of nvH1N1 infection. The cytokine storm can result in acute lung injury and further progress to ARDS. This is characterized by local infiltration of inflammatory cells, increased vascular permeability and systemic spillover of inflammatory mediators that can cause systemic sepsis-like symptoms [23]. While focus on cytokine storm detection relies mostly on measuring cytokines in the systemic circulation, it has been suggested that measuring systemic inflammatory mediators may underestimate the extent of the immunological cascade that takes place locally in deep tissues such as the respiratory tract [23]. Considering the above, controlling the inflammatory response may be an effective way of preventing collateral damage caused by the excessive activation of the immune system to clear pathogens.
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3. Cholinergic anti-inflammatory pathway
Since the early 2000s, the cholinergic nervous system has been identified as an important pathway that modifies and controls the inflammatory response.
Surgical dissection of the vagus nerve in mice led to enhanced TNF production and excessive response to endotoxin administration, while vagus nerve electrical stimulation inhibits the synthesis of TNF and prevents the acute inflammatory response [[24], [25], [26]]. Several animal experimental models inducing pro-inflammatory cytokines, such as sepsis, ischemia-reperfusion and pancreatitis have shown that vagus stimulation improves outcomes. This effect is mediated by the nicotinic acetylcholine receptor (nAChR) α7 subunit on macrophages [27]. Mice deficient of the α7 subunit exhibited increased endotoxin-induced TNF production, and electrical vagus innervation failed to reduce serum TNF levels [27]. B-lymphocytes also express α7 nAChRs. Macrophages appear to be very sensitive to acetylcholine, which suggests that any source of acetylcholine, even from non-neuronal sources such as epithelial and endothelial cells, could also modulate the activity of adjacent macrophages [25]. Besides TNF, other pro-inflammatory cytokines are inhibited by acetylcholine, such as high mobility group B1 (HMGB1), IL-1, and IL-6 [28].
Modulation of inflammatory and immune response by the central nervous system (CNS) through the vagus nerve is based on bi-directional communication between the immune and nervous systems. Afferent vagus nerve fibers, located in nucleus tractus solitarius, provide sensory input to the CNS about the inflammatory status that can result in the transmission of efferent signals, originating from the dorsal motor nucleus, to control the inflammatory response [29]. Such a response is rapid and localized, unlike the diffusible anti-inflammatory network, which is slow, distributed, non-integrated and dependent on concentration gradients [25].
Part 1 of 3
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marsh
On TB every waking moment
4. Nicotine, nicotinic cholinergic system and COVID-19
Smoking is known to increase the risk for respiratory infection susceptibility and severity [30,31]. Considering that COVID-19 was declared by the World Health Organization as a pandemic, a substantial disease burden would be expected among the estimated 1.1 billion smokers, especially in countries with high smoking prevalence. Therefore, there were understandable concerns about this population subgroup [32]. Additionally, smoking-related disease conditions such as cardiovascular disease and COPD are also established risk factors for adverse outcomes in COVID-19 [33]. China was the first country to be affected by the pandemic and has a high smoking prevalence. In 2018, the population smoking prevalence was 26.6 % with a much higher prevalence in men (50.5 %) than in women (2.1 %) [34]. Therefore, a high smoking prevalence among patients with COVID-19 would be expected, even if smoking did not adversely affect disease susceptibility and severity.
On 23 March, a preliminary analysis by some members of our group examined data from 5 case series of hospitalized COVID-19 patients from China, and calculated a smoking prevalence of 10.2 % (95 % CI: 8.7–11.8 %) while the estimated expected prevalence was 31.3 % (95 % CI: 8.7–11.8 %) [35]. The analysis was further expanded on 3 April by examining 13 Chinese studies and 5960 hospitalized COVID-19 patients, with a pooled smoking prevalence of 6.5 % (95 % CI: 4.9–8.2 %) [36]. On that date, we presented for the first time a hypothesis about the potential beneficial effects of nicotine, which was subsequently expanded [37]. While there were limitations in the study analysis, mainly due to the inability to adjust for confounding factors, the findings of low smoking prevalence among hospitalized COVID-19 patients in China were consistent across all studies and in agreement with case series from USA [38,39]. The original hypothesis was based on the anti-inflammatory properties of nicotine through the cholinergic anti-inflammatory system, acknowledging that the disease appeared to involve a dysregulation of the immune response to viral invasion.
It is obviously inappropriate to suggest that anyone should initiate smoking or continue to smoke, due to the well-established smoking-related morbidities and the large number of toxic chemicals in cigarette smoke. Furthermore, it is unlikely that any other compound in tobacco cigarette smoke, besides nicotine, would be implicated to the potential benefits observed in smokers. Moreover, due to the adverse effects of smoking and the fact that many smokers would suffer from co-morbidities (such as cardiovascular disease, COPD etc.), it is expected that the potential benefits of nicotine would be masked by the adverse effects of smoking.
Nicotine is a cholinergic agonist. Therefore, it is an important inhibitor of pro-inflammatory cytokines acting through the cholinergic anti-inflammatory pathway via α7-nAChRs. Nicotine inhibits TNF, IL-1, IL-6 and HMGB1 while it does not inhibit anti-inflammatory cytokines such as IL-10 [28]. In vivo animal models have found nicotine to be protective against lipopolysaccharide-induced ARDS by reducing leukocyte infiltration and pro-inflammatory mediators in bronchoalveolar lavage fluid [40]. Such effects are relevant to COVID-19 since cytokine storm appears to be the hallmark in severe cases [41,42]. Several pro-inflammatory cytokines, such as IL-1β, IL-2, IL-6, IL-17, IL-8, TNF and CCL2 are elevated in COVID-19 patients [43]. Treatment with anti-IL-6 anti-TNF medications has been proposed and clinical trials are already underway [44,45]. However, it may be more effective to inhibit several instead of selectively one cytokine, while some cytokine inhibitors are associated with elevated risk of opportunistic infections [46]. Also, it is possible that measuring blood levels of inflammatory cytokines does not accurately reflect the extent of the immune imbalance that exists locally in the lungs. In any case, the cholinergic anti-inflammatory system could provide better control and modulation of the cytokine response compared to blocking a single agent, and nicotine could effectively contribute to maintaining a balanced immune response against viral infection. Therefore, it is possible that the clinical manifestations of cytokine storm in COVID-19 patients are the result of dysfunction of the cholinergic anti-inflammatory pathway.
SARS-CoV-2 is known to use the angiotensin converting enzyme 2 (ACE2) as a receptor for cell entry [47]. ACE2 has well-established vasodilatory, anti-inflammatory and antioxidant properties. Studies on smoking and ACE2 have reported contradictory findings. Studies published before the COVID-19 pandemic reported that smoking and nicotine down-regulate ACE2 [48,49]. However, more recent studies suggest that they up-regulate ACE2 [[50], [51], [52]]. There is currently no evidence to suggest that up-regulation of ACE2 is associated with increased COVID-19 susceptibility or severity. In fact, up-regulation of ACE2 appears to be protective against tissue damage caused by SARS-CoV-2. ACE2 has been found to protect mice from developing ARDS [[53], [54], [55]]. Data from SARS experimental studies suggest that continuous SARS-CoV-2 infection and replication induces immediate down-regulation of ACE2 that may be implicated in organ damage and disease severity [56]. Further support for the beneficial role of ACE2 comes from data that estrogens appear to up-regulate ACE2 while children and younger adults have higher ACE2 levels compared to older people [57,58]. At the same time, women, children and young people have milder COVID-19 symptoms. If accurate and verified, the recently-observed ACE2 up-regulation in smokers is probably induced as a defence mechanism to counteract the effects of angiotensin II. There is probably a dynamic balance between ACE and ACE2, which is continuously changing, depending on stressors and stimuli. Thus, there is uncertainty on whether nicotine affects COVID-19 progression through the renin-angiotensin-aldosterone axis and there is no known interaction between ACE2 and nAChR receptors.
Importantly, ACE2 is expressed in several regions in the brain. The regions where vagal afferent fibers terminate and vagal efferent fibers originate exhibit ACE2 expression [59,60]. Neuroinvasion is a common feature of coronaviruses [61]. Anosmia and ageusia have been reported by COVID-19 patients [62]. SARS-CoV-2 may enter the CNS either through the blood stream or via the olfactory nerve across the cribriform plate [63,64]. A case series of 214 patients reported that 36.4 % had neurological manifestations [65]. Thus, it is possible that the virus might infect the terminal areas of vagus afferent fibers or the origin of vagus efferent fiber causing down-regulation of ACE2 and resulting in local inflammation that could disrupt the cholinergic anti-inflammatory pathway and dysregulate the inflammatory response. Nicotine could have protective properties against possible brain inflammation caused by SARS-CoV-2, mediated through α7-AChRs [66].
A noteworthy parameter relative to anosmia and ageusia observed among COVID-19 patients is that these are characteristic and prodromal non-motor manifestations of Parkinson’s disease [67,68]. While ageusia has not been extensively studied, olfactory disturbance is a very common feature, observed in up to 95 % of Parkinson’s disease patients [68], and may appear several years before the onset of motor symptoms. There is no olfactory improvement with dopamine agonists [69,70]. Unlike the general population where smoking is associated with impaired olfactory function, smokers with Parkinson’s disease experience less decline in olfactory sense compared to non-smokers, suggesting a protective effect of smoking [71]. This maybe explained by the fact olfactory loss has been linked to impairment of cholinergic transmission [72] while nicotine improved the olfactory impairment in a mouse model of Parkinson’s disease [73]. The olfactory bulb has a rich network of nAChRs, but α7 nAChRs may also be expressed on the axon terminals of the olfactory receptor neurons [74]. While this may suggest facilitated brain infection through anterograde transport along the olfactory nerve, it is possible that olfactory receptor neurons may act as first-line viral sensors and initiate a rapid immune response [75]. This would explain the mild symptoms in COVID-19 patients with olfactory loss. In any case, anosmia may represent another sign of dysfunction of the nicotinic cholinergic system in COVID-19.
A prominent feature of COVID-19 is coagulopathy that results in thromboembolic complications. Venous thromboembolism was reported in 25 % of patients who were not under thromboprophylaxis, and was associated with higher mortality rate [76]. Abnormal coagulation parameters were also associated with poor survival [77]. Although venous thromboembolism is a well-known complication of any serious infection, additional mechanisms such as endothelial damage, increased vascular permeability and microvascular occlusion may be implicated in COVID-19 [78]. It is important to note that platelets express functional α7-AChRs [79] while hematopoietic α7 nAChR deficiency increases inflammation and platelet activity [80]. Recently, acetylcholine was found to be an endogenous inhibitor of platelet activation [81]. Therefore, dysfunction of the nicotinic cholinergic system could be implicated in the thrombotic and vascular complications of COVID-19.
Go to:
Part 2 of 3
Smoking is known to increase the risk for respiratory infection susceptibility and severity [30,31]. Considering that COVID-19 was declared by the World Health Organization as a pandemic, a substantial disease burden would be expected among the estimated 1.1 billion smokers, especially in countries with high smoking prevalence. Therefore, there were understandable concerns about this population subgroup [32]. Additionally, smoking-related disease conditions such as cardiovascular disease and COPD are also established risk factors for adverse outcomes in COVID-19 [33]. China was the first country to be affected by the pandemic and has a high smoking prevalence. In 2018, the population smoking prevalence was 26.6 % with a much higher prevalence in men (50.5 %) than in women (2.1 %) [34]. Therefore, a high smoking prevalence among patients with COVID-19 would be expected, even if smoking did not adversely affect disease susceptibility and severity.
On 23 March, a preliminary analysis by some members of our group examined data from 5 case series of hospitalized COVID-19 patients from China, and calculated a smoking prevalence of 10.2 % (95 % CI: 8.7–11.8 %) while the estimated expected prevalence was 31.3 % (95 % CI: 8.7–11.8 %) [35]. The analysis was further expanded on 3 April by examining 13 Chinese studies and 5960 hospitalized COVID-19 patients, with a pooled smoking prevalence of 6.5 % (95 % CI: 4.9–8.2 %) [36]. On that date, we presented for the first time a hypothesis about the potential beneficial effects of nicotine, which was subsequently expanded [37]. While there were limitations in the study analysis, mainly due to the inability to adjust for confounding factors, the findings of low smoking prevalence among hospitalized COVID-19 patients in China were consistent across all studies and in agreement with case series from USA [38,39]. The original hypothesis was based on the anti-inflammatory properties of nicotine through the cholinergic anti-inflammatory system, acknowledging that the disease appeared to involve a dysregulation of the immune response to viral invasion.
It is obviously inappropriate to suggest that anyone should initiate smoking or continue to smoke, due to the well-established smoking-related morbidities and the large number of toxic chemicals in cigarette smoke. Furthermore, it is unlikely that any other compound in tobacco cigarette smoke, besides nicotine, would be implicated to the potential benefits observed in smokers. Moreover, due to the adverse effects of smoking and the fact that many smokers would suffer from co-morbidities (such as cardiovascular disease, COPD etc.), it is expected that the potential benefits of nicotine would be masked by the adverse effects of smoking.
Nicotine is a cholinergic agonist. Therefore, it is an important inhibitor of pro-inflammatory cytokines acting through the cholinergic anti-inflammatory pathway via α7-nAChRs. Nicotine inhibits TNF, IL-1, IL-6 and HMGB1 while it does not inhibit anti-inflammatory cytokines such as IL-10 [28]. In vivo animal models have found nicotine to be protective against lipopolysaccharide-induced ARDS by reducing leukocyte infiltration and pro-inflammatory mediators in bronchoalveolar lavage fluid [40]. Such effects are relevant to COVID-19 since cytokine storm appears to be the hallmark in severe cases [41,42]. Several pro-inflammatory cytokines, such as IL-1β, IL-2, IL-6, IL-17, IL-8, TNF and CCL2 are elevated in COVID-19 patients [43]. Treatment with anti-IL-6 anti-TNF medications has been proposed and clinical trials are already underway [44,45]. However, it may be more effective to inhibit several instead of selectively one cytokine, while some cytokine inhibitors are associated with elevated risk of opportunistic infections [46]. Also, it is possible that measuring blood levels of inflammatory cytokines does not accurately reflect the extent of the immune imbalance that exists locally in the lungs. In any case, the cholinergic anti-inflammatory system could provide better control and modulation of the cytokine response compared to blocking a single agent, and nicotine could effectively contribute to maintaining a balanced immune response against viral infection. Therefore, it is possible that the clinical manifestations of cytokine storm in COVID-19 patients are the result of dysfunction of the cholinergic anti-inflammatory pathway.
SARS-CoV-2 is known to use the angiotensin converting enzyme 2 (ACE2) as a receptor for cell entry [47]. ACE2 has well-established vasodilatory, anti-inflammatory and antioxidant properties. Studies on smoking and ACE2 have reported contradictory findings. Studies published before the COVID-19 pandemic reported that smoking and nicotine down-regulate ACE2 [48,49]. However, more recent studies suggest that they up-regulate ACE2 [[50], [51], [52]]. There is currently no evidence to suggest that up-regulation of ACE2 is associated with increased COVID-19 susceptibility or severity. In fact, up-regulation of ACE2 appears to be protective against tissue damage caused by SARS-CoV-2. ACE2 has been found to protect mice from developing ARDS [[53], [54], [55]]. Data from SARS experimental studies suggest that continuous SARS-CoV-2 infection and replication induces immediate down-regulation of ACE2 that may be implicated in organ damage and disease severity [56]. Further support for the beneficial role of ACE2 comes from data that estrogens appear to up-regulate ACE2 while children and younger adults have higher ACE2 levels compared to older people [57,58]. At the same time, women, children and young people have milder COVID-19 symptoms. If accurate and verified, the recently-observed ACE2 up-regulation in smokers is probably induced as a defence mechanism to counteract the effects of angiotensin II. There is probably a dynamic balance between ACE and ACE2, which is continuously changing, depending on stressors and stimuli. Thus, there is uncertainty on whether nicotine affects COVID-19 progression through the renin-angiotensin-aldosterone axis and there is no known interaction between ACE2 and nAChR receptors.
Importantly, ACE2 is expressed in several regions in the brain. The regions where vagal afferent fibers terminate and vagal efferent fibers originate exhibit ACE2 expression [59,60]. Neuroinvasion is a common feature of coronaviruses [61]. Anosmia and ageusia have been reported by COVID-19 patients [62]. SARS-CoV-2 may enter the CNS either through the blood stream or via the olfactory nerve across the cribriform plate [63,64]. A case series of 214 patients reported that 36.4 % had neurological manifestations [65]. Thus, it is possible that the virus might infect the terminal areas of vagus afferent fibers or the origin of vagus efferent fiber causing down-regulation of ACE2 and resulting in local inflammation that could disrupt the cholinergic anti-inflammatory pathway and dysregulate the inflammatory response. Nicotine could have protective properties against possible brain inflammation caused by SARS-CoV-2, mediated through α7-AChRs [66].
A noteworthy parameter relative to anosmia and ageusia observed among COVID-19 patients is that these are characteristic and prodromal non-motor manifestations of Parkinson’s disease [67,68]. While ageusia has not been extensively studied, olfactory disturbance is a very common feature, observed in up to 95 % of Parkinson’s disease patients [68], and may appear several years before the onset of motor symptoms. There is no olfactory improvement with dopamine agonists [69,70]. Unlike the general population where smoking is associated with impaired olfactory function, smokers with Parkinson’s disease experience less decline in olfactory sense compared to non-smokers, suggesting a protective effect of smoking [71]. This maybe explained by the fact olfactory loss has been linked to impairment of cholinergic transmission [72] while nicotine improved the olfactory impairment in a mouse model of Parkinson’s disease [73]. The olfactory bulb has a rich network of nAChRs, but α7 nAChRs may also be expressed on the axon terminals of the olfactory receptor neurons [74]. While this may suggest facilitated brain infection through anterograde transport along the olfactory nerve, it is possible that olfactory receptor neurons may act as first-line viral sensors and initiate a rapid immune response [75]. This would explain the mild symptoms in COVID-19 patients with olfactory loss. In any case, anosmia may represent another sign of dysfunction of the nicotinic cholinergic system in COVID-19.
A prominent feature of COVID-19 is coagulopathy that results in thromboembolic complications. Venous thromboembolism was reported in 25 % of patients who were not under thromboprophylaxis, and was associated with higher mortality rate [76]. Abnormal coagulation parameters were also associated with poor survival [77]. Although venous thromboembolism is a well-known complication of any serious infection, additional mechanisms such as endothelial damage, increased vascular permeability and microvascular occlusion may be implicated in COVID-19 [78]. It is important to note that platelets express functional α7-AChRs [79] while hematopoietic α7 nAChR deficiency increases inflammation and platelet activity [80]. Recently, acetylcholine was found to be an endogenous inhibitor of platelet activation [81]. Therefore, dysfunction of the nicotinic cholinergic system could be implicated in the thrombotic and vascular complications of COVID-19.
Go to:
Part 2 of 3
Last edited:
marsh
On TB every waking moment
5. COVID-19 could be a disease of the nicotinic cholinergic system
The observation of a low prevalence of hospitalized COVID-19 patients in China led to the development of a hypothesis that nicotine could have protective effects by enhancing the cholinergic anti-inflammatory pathway [36]. As more studies presented the clinical manifestations, laboratory findings and disease progression in COVID-19 patients, it became apparent that the nicotinic cholinergic system could explain most (if not all) of the disease characteristics. It would be unlikely for a single “defence system” to ameliorate all the diverse and complex manifestations of COVID-19, unless that “defence mechanism” was the target of the viral host. Could that be possible?
SARS-CoV-2 appears to have originated from a bat coronavirus. Ji et al. [82] carried out comprehensive sequence analysis in conjunction with relative synonymous codon usage bias and reported that the virus may have been a recombinant virus between the bat coronavirus and an unknown-origin coronavirus [83]. One possible intermediate host could have been a snake. Taking into consideration that snake venom toxins are competitive antagonists of acetylcholine on α7-nACh receptor with high affinity, we decided to explore the hypothesis that SARS-CoV-2 may have acquired sequences by any of the potential, and not defined yet, intermediates through genomic recombination. We compared the protein sequences between SARS-CoV-2 and snake venom neurotoxins. We were able to identify regions with four or five amino acids identity between the coronavirus and several neurotoxin molecules (e.g. SARS-CoV-2 compared with Muscarinic toxin like protein, Fig. 1A; SARS-CoV-2 and Cobrotoxin - Naja siamensis, Fig. 1B).
Therefore, we hypothesize that these, or other, sequences on the SARS-CoV-2 proteins, being similar to the active sites of a neurotoxin, can result in binding to nAChRs and may adversely affect their function by preventing the action of acetylcholine.
6. Nicotine as a potential treatment for COVID-19
Nicotine could act as a competitive agonist for the nAChRs that could restore the compromised function of the nicotinic cholinergic system. This may be feasible through repurposing already approved (for other indications) pharmaceutical nicotine products such as nicotine patches for use by non-smokers, or even by using these products as already indicated (i.e. as smoking substitutes) among current smokers. These products are available over-the-counter in most countries. They have been administered therapeutically in non-smokers for neurological conditions and inflammatory bowel disease for larger periods than would be needed for COVID-19 [[83], [84], [85]]. No abuse liability was observed in non-smokers despite being administerd for several weeks [84,85]. Besides gums and patches, nicotine can be administered though inhalation, with the use of a nebulizer or other aerosol systems, if necessary. Nicotine administration could be added on top of antiviral or other therapeutic options for COVID-19. By restoring and re-activating the cholinergic anti-inflammatory pathway, a more universal suppression of the cytokine storm could probably be achieved compared to administering inhibitors of a single cytokine. The potential need to provide pharmaceutical nicotine products to smokers and users of other nicotine products who experience abrupt nicotine cessation when hospitalized for COVID-19 or aim to follow medical advice to quit smoking, should also be examined. If the hypothesis about the beneficial effects of nicotine is valid, smokers who quit nicotine use when hospitalized will be deprived from these benefits. In France, the Addiction Prevention Network (RESPADD) officially recommends the use of nicotine replacement therapies for smokers when hospitalized for any illness [86]. Clinical trials will dictate future approaches and the role of nicotine in COVID-19, while further experimental studies should examine the affinity of the virus to nAChRs.
Go to:
7. Conclusions
In conclusion, we noticed that most of the clinical characteristics of severe COVID-19 could be explained by dysregulation of the cholinergic anti-inflammatory pathway. The observation that patients eventually develop cytokine storm which results in rapid clinical deterioration, led to the development of a hypothesis about the series of events associated with adverse outcomes in COVID-19 (Fig. 2).
Fig. 2
Progression of COVID-19 after SARS-CoV-2 infection.
Once someone is infected with SARS-CoV-2, the immune system is mobilized. As the virus replicates, cell and viral debris or virions may interact with the nAChRs blocking the action of the cholinergic anti-inflammatory pathway. If the initial immune response is not enough to combat the viral invasion at an early stage, the extensive and prolonged replication of the virus will eventually disrupt the cholinergic anti-inflammatory pathway seriously compromising its ability to control and regulate the immune response. The uncontrolled action of pro-inflammatory cytokines will result in the development of cytokine storm, with acute lung injury leading to ARDS, coagulation disturbances and multiorgan failure. Based on this hypothesis, COVID-19 appears to eventually become a disease of the nicotinic cholinergic system. Nicotine could maintain or restore the function of the cholinergic anti-inflammatory system and thus control the release and activity of pro-inflammatory cytokines. This could prevent or suppress the cytokine storm. This hypothesis needs to be examined in the laboratory and the clinical setting.
3 of 3 see URL for references
The observation of a low prevalence of hospitalized COVID-19 patients in China led to the development of a hypothesis that nicotine could have protective effects by enhancing the cholinergic anti-inflammatory pathway [36]. As more studies presented the clinical manifestations, laboratory findings and disease progression in COVID-19 patients, it became apparent that the nicotinic cholinergic system could explain most (if not all) of the disease characteristics. It would be unlikely for a single “defence system” to ameliorate all the diverse and complex manifestations of COVID-19, unless that “defence mechanism” was the target of the viral host. Could that be possible?
SARS-CoV-2 appears to have originated from a bat coronavirus. Ji et al. [82] carried out comprehensive sequence analysis in conjunction with relative synonymous codon usage bias and reported that the virus may have been a recombinant virus between the bat coronavirus and an unknown-origin coronavirus [83]. One possible intermediate host could have been a snake. Taking into consideration that snake venom toxins are competitive antagonists of acetylcholine on α7-nACh receptor with high affinity, we decided to explore the hypothesis that SARS-CoV-2 may have acquired sequences by any of the potential, and not defined yet, intermediates through genomic recombination. We compared the protein sequences between SARS-CoV-2 and snake venom neurotoxins. We were able to identify regions with four or five amino acids identity between the coronavirus and several neurotoxin molecules (e.g. SARS-CoV-2 compared with Muscarinic toxin like protein, Fig. 1A; SARS-CoV-2 and Cobrotoxin - Naja siamensis, Fig. 1B).
Therefore, we hypothesize that these, or other, sequences on the SARS-CoV-2 proteins, being similar to the active sites of a neurotoxin, can result in binding to nAChRs and may adversely affect their function by preventing the action of acetylcholine.
6. Nicotine as a potential treatment for COVID-19
Nicotine could act as a competitive agonist for the nAChRs that could restore the compromised function of the nicotinic cholinergic system. This may be feasible through repurposing already approved (for other indications) pharmaceutical nicotine products such as nicotine patches for use by non-smokers, or even by using these products as already indicated (i.e. as smoking substitutes) among current smokers. These products are available over-the-counter in most countries. They have been administered therapeutically in non-smokers for neurological conditions and inflammatory bowel disease for larger periods than would be needed for COVID-19 [[83], [84], [85]]. No abuse liability was observed in non-smokers despite being administerd for several weeks [84,85]. Besides gums and patches, nicotine can be administered though inhalation, with the use of a nebulizer or other aerosol systems, if necessary. Nicotine administration could be added on top of antiviral or other therapeutic options for COVID-19. By restoring and re-activating the cholinergic anti-inflammatory pathway, a more universal suppression of the cytokine storm could probably be achieved compared to administering inhibitors of a single cytokine. The potential need to provide pharmaceutical nicotine products to smokers and users of other nicotine products who experience abrupt nicotine cessation when hospitalized for COVID-19 or aim to follow medical advice to quit smoking, should also be examined. If the hypothesis about the beneficial effects of nicotine is valid, smokers who quit nicotine use when hospitalized will be deprived from these benefits. In France, the Addiction Prevention Network (RESPADD) officially recommends the use of nicotine replacement therapies for smokers when hospitalized for any illness [86]. Clinical trials will dictate future approaches and the role of nicotine in COVID-19, while further experimental studies should examine the affinity of the virus to nAChRs.
Go to:
7. Conclusions
In conclusion, we noticed that most of the clinical characteristics of severe COVID-19 could be explained by dysregulation of the cholinergic anti-inflammatory pathway. The observation that patients eventually develop cytokine storm which results in rapid clinical deterioration, led to the development of a hypothesis about the series of events associated with adverse outcomes in COVID-19 (Fig. 2).
Fig. 2
Progression of COVID-19 after SARS-CoV-2 infection.
Once someone is infected with SARS-CoV-2, the immune system is mobilized. As the virus replicates, cell and viral debris or virions may interact with the nAChRs blocking the action of the cholinergic anti-inflammatory pathway. If the initial immune response is not enough to combat the viral invasion at an early stage, the extensive and prolonged replication of the virus will eventually disrupt the cholinergic anti-inflammatory pathway seriously compromising its ability to control and regulate the immune response. The uncontrolled action of pro-inflammatory cytokines will result in the development of cytokine storm, with acute lung injury leading to ARDS, coagulation disturbances and multiorgan failure. Based on this hypothesis, COVID-19 appears to eventually become a disease of the nicotinic cholinergic system. Nicotine could maintain or restore the function of the cholinergic anti-inflammatory system and thus control the release and activity of pro-inflammatory cytokines. This could prevent or suppress the cytokine storm. This hypothesis needs to be examined in the laboratory and the clinical setting.
3 of 3 see URL for references
Last edited:
Heliobas Disciple
TB Fanatic
Here's some info on how often you'd have to take the vaccine if they come up with one.
End Of The American Dream
Life As You Have Known It Will Never Be The Same Again...
endoftheamericandream.com
An Experimental COVID-19 Vaccine Being Rushed Through Development Will Require More Than One Injection
Michael Snyder
July 14, 2020
A lot of Americans are assuming that eventually a newly developed COVID-19 vaccine will put an end to this pandemic. And many of those same people are assuming that all they will have to do is get one shot and they will be protected from the virus for their rest of their lives. Unfortunately, that is not the way that it is going to work. As you will see below, the experimental vaccine that is making the most headlines will require two shots, and those two shots will be a month apart. And because COVID-19 antibodies disappear in just a few months, those that get the vaccine will need a “booster shot” very rapidly after the first two injections, and then another one, and then another one, and then more “booster shots” at regular intervals in perpetuity. Of course most Americans won’t want to submit to an endless series of shots that only provide very brief periods of protection at best, but authorities will be very strongly pushing people to do so.
The experimental vaccine that I am referring to is being developed by Moderna, and data from the phase 1 clinical trial was published on Tuesday…
Also Tuesday, Moderna published data from its phase 1 clinical trial in the New England Journal of Medicine.
That trial, which involved 45 participants, was meant to test a new drug’s safety, not its effectiveness. But the company said results from all 45 participants showed they developed antibodies key to fighting the virus at levels up to four times the amount found in patients who got sick and then recovered from the virus.
Many analysts were encouraged by these results, and the stock market soared.
But one expert that was interviewed by NBC News cautioned that the clinical trial did not show if the antibodies actually lead to immunity, and it also did not show how long such immunity would last…
Gonsenhauser, who is not involved with any COVID-19 vaccine research, cautioned that while the findings are promising, scientists have not yet shown that COVID-19 antibodies lead to immunity, and if so, how long that immunity lasts.
What we do know is that three separate studies have now shown that COVID-19 antibodies fade very, very rapidly for those that have tested positive for the virus. In fact, some victims no longer test positive for antibodies after just a few weeks.
If a COVID-19 vaccine produces “immunity” that only lasts for “a few weeks”, it will essentially be completely worthless.
And we also know that an increasing number of Americans appear to be catching COVID-19 again very quickly after their first battle with the virus. For example, NBC News recently featured the case of 56-year-old nurse Sherry Wellman of Youngstown, Ohio…
After an initial positive test for the virus in March, two additional COVID-19 tests in April were negative. It was welcome news to Wellman, whose job as a nurse required her to have two negative tests before returning to work.
But a month later, she had to go to the hospital for chest pains, and was tested again.
And guess what?
The test showed that she had COVID-19 once again.
There have been many other cases such as this, and I included a few of them in a recent article. A lot of people may not want to hear this, but just like other coronaviruses you can catch COVID-19 over and over again.
A COVID-19 vaccine is probably the most anticipated vaccine in modern American history, and right now there is a worldwide race to produce one that is safe and effective. President Trump has launched “Operation Warp Speed” in an effort to have the U.S. be the first one to produce a vaccine, and right now it appears that the experimental Moderna vaccine is the most promising candidate. According to Yahoo News, the Moderna vaccine will require “two doses”…
The vaccine requires two doses, a month apart.
So that means two separate trips to the doctor, and a lot of Americans are not going to be excited about that.
At this point, we do not know if the Moderna vaccine will be effective, and we certainly don’t know if it will be safe.
In the clinical trial, “more than half the study participants” reported some very alarming side effects…
There were no serious side effects. But more than half the study participants reported flu-like reactions to the shots that aren’t uncommon with other vaccines — fatigue, headache, chills, fever and pain at the injection site. For three participants given the highest dose, those reactions were more severe; that dose isn’t being pursued.
Don’t you love how they claim that there were “no serious side effects” and then they go on to list a whole bunch of very serious side effects that were reported by more than half the people in the study?
To me, if a shot gives you “fatigue, headache, chills, fever and pain”, that is a major red flag.
But one “vaccine expert” says that such side effects are “a small price to pay”…
“Small price to pay for protection against COVID,” said Dr. William Schaffner of Vanderbilt University Medical Center, a vaccine expert who wasn’t involved with the study.
Of course vaccine safety advocates have been told similar things for decades when confronting the industry with horrific stories of vaccine side effects.
Rushing a vaccine through the development process is a very, very bad idea, and it is imperative that safety concerns be fully addressed.
Because we certainly do not want a vaccine pushed on the American public that will do even more damage than the virus itself is doing.
And of course there are tens of millions of Americans that will not want to take any COVID-19 vaccine under any circumstances.
But there will be lots of people that will line up for the shots as soon as they are available, and most of them will assume that the shots will provide long-term protection.
However, it is extremely unlikely that any vaccine will produce as much immunity as actually having the disease does, and at this point we know that actually having the virus produces only a few months of immunity at best.
So the truth is that all of this hope that a “vaccine” will end this pandemic is likely just a mirage, but the mainstream media will likely attempt to keep this mirage going for as long as possible.
.
Last edited:
Heliobas Disciple
TB Fanatic
(fair use applies)
Mystery as Argentine sailors infected with virus after 35 days at sea
Argentina is trying to solve a medical mystery after 57 sailors were infected with the coronavirus after 35 days at sea, despite the entire crew testing negative before leaving port. The Echizen Maru fishing trawler returned to port after some of its crew began exhibiting symptoms typical of...news.yahoo.com
Mystery as Argentine sailors infected with virus after 35 days at sea
July 13, 2020, 11:57 pm
Argentina is trying to solve a medical mystery after 57 sailors were infected with the coronavirus after 35 days at sea, despite the entire crew testing negative before leaving port.
The Echizen Maru fishing trawler returned to port after some of its crew began exhibiting symptoms typical of COVID-19, the health ministry for the southern Tierra del Fuego province said Monday.
According to the ministry, 57 sailors, out of 61 crew members, were diagnosed with the virus after undergoing a new test.
However, all of the crew members had undergone 14 days of mandatory quarantine at a hotel in the city of Ushuaia. Prior to that, they had negative results, the ministry said in a statement.
Two of the other sailors have tested negative, and two others are awaiting test results, the province's emergency operations committee said.
Two sailors were hospitalized.
"It's hard to establish how this crew was infected, considering that for 35 days, they had no contact with dry land and that supplies were only brought in from the port of Ushuaia," said Alejandra Alfaro, the director of primary health care in Tierra del Fuego.
A team was examining "the chronology of symptoms in the crew to establish the chronology of contagion," she said.
The head of the infectious diseases department at Ushuaia Regional Hospital, Leandro Ballatore, said he believed this is a "case that escapes all description in publications, because an incubation period this long has not been described anywhere."
"We cannot yet explain how the symptoms appeared," said Ballatore.
The crew was placed in isolation on board the ship and returned to the port of Ushuaia.
Argentina exceeded 100,000 total cases on Sunday, and the death toll rose to 1,859. The majority of infections are in the Buenos Aires area.
I don't think they know. I think something similar happened at the beginning of the pandemic, in March or April, where sailors on a ship got sick after being all clear. My hypothesis is this disease can hibernate in your body and show up when something triggers it. Just my theory, probably way off base.
HD
Heliobas Disciple
TB Fanatic
That's a good idea. Also buy masks when you see them now in case you can't get them later. It's something to stock up on.
HD
Heliobas Disciple
TB Fanatic
There are a lot of graphs for various states on this page, go to the link if you want to see them, it's too many to transfer over.
www.dailymail.co.uk
(fair use applies)
Coronavirus deaths are up 46% across the US in the last week with Texas, Arizona and Mississippi reporting the biggest weekly spikes - as 46 states continue to record new cases
By Emily Crane
Published: 09:10 EDT, 14 July 2020 | Updated: 12:32 EDT, 14 July 2020
Deaths related to COVID-19 have increased across the United States by 46 percent in the past week with Texas, Arizona and Mississippi reporting the biggest weekly spikes.
More than 5,000 people died from COVID-19 between July 6 and July 12, which is an increase of 46 percent compared to the previous week, according to a Reuters analysis of data from The COVID Tracking Project.
About a dozen states have reported increases in deaths for at least two straight weeks, including California, Florida and Texas.
In Texas, news deaths surged by 127 percent last week when it added 555 new deaths, bringing the total to just over 3,100.
Arizona's deaths increased by 94 percent after adding 428 deaths. The hardhit state's death toll was at 2,237 the week ending July 12.
Mississippi's deaths spike by 92 percent last week compared to the previous week. The state added 138 deaths, bringing the total to just over 1,200.
In California and Florida - two of the other hot spot states - deaths surged by more than 60 percent last week.
Florida recorded 514 deaths in the week ending July 12, bringing total to over 4,300; and California reported 686 deaths, bringing the total to 7,000. Florida on Monday added a record 132 fatalities to its death toll.
New cases also continue to rise with the US reporting over 400,000 infections for the week ending July 12, which was up 21 percent from the previous seven days.
Nationally, new COVID-19 cases have risen every week for six straight weeks.
Forty-six states reported more new cases of COVID-19 last week compared to the previous week, the analysis found.
Cases are only falling on a weekly basis in New York, Tennessee, New Jersey and Delaware.
While Southern and Western states are seeing the biggest increase in cases, infections are also rising in the Midwest with Minnesota cases up 60 percent, Missouri up 40 percent and Iowa up 30 percent.
Currently, more than 135,000 Americans have died from coronavirus and there have been more than 3.3 million infections.
Until now, the number of deaths per day from COVID-19 had been falling for months even as hot spots states like Florida, Texas and Arizona saw explosions in cases and hospitalizations.
Daily infections across the US have broken records several times in recent days.
Health officials have been warning for weeks that deaths would surge again because the fatality rate lags several weeks behind infections.
A coronavirus death, when it occurs, typically comes several weeks after a person is first infected.
Experts had predicted states that saw spikes in cases and hospitalizations would, at some point, see deaths rise too.
The impact of the new surge in deaths has been felt by the healthcare workers grappling in overstretched hospitals with Texas and Arizona requesting refrigerated trucks as morgues reach capacity.
In Arizona, capacity within intensive care units had surged to 90 percent. Hospitalizations in Texas continue to spike to record highs with more than 10,000 people being treated on Monday.
Researchers expect deaths to rise for at least several weeks but some think the count probably will not go up as dramatically as it did in the spring.
A forecast model from the University of Washington's Institute for Health Metrics is predicting the death toll to rise to 208,255 by November 1.
Experts say the death toll may not be as bad as when the pandemic first hit because testing was extremely limited early on and that many people's health behaviors have now changed with mask-wearing becoming more common in some places.
Testing for COVID-19 rose by 7.4 percent in the United States last week and set a new record high on July 10, with over 823,000 tests performed, according to the Reuters analysis.
Nationally, 8.8 percent of tests came back positive for coronavirus, up from 7.5 percent the prior week and 5 percent three weeks ago.
The World Health Organization considers a positivity rate above 5 percent to be a cause for concern because it suggests there are more cases in the community that have not yet been uncovered.
Thirty-one states had positivity test rates above 5 percent, according to the analysis, including Arizona at 27 percent, South Carolina at 19 percent and Florida at 19 percent.
The surge in new cases has prompted many states to temporarily halt the reopening of their economies or order some businesses to close for a second time.
California's Gov Gavin Newsom has once again closed bars, inside dining and, for much of the state, gyms, indoor church services and hair and nail salons in an effort to prevent COVID-19 cases from swamping hospitals.
The Gov issued the sweeping set of closures on Monday as the state recorded more than 329,000 cases and deaths topped 7,000. Hospitalizations have surged by 28 percent in the past two weeks, including a 20 percent increase in patients requiring intensive care.
'COVID-19 is not going away anytime soon, until there is a vaccine and or an effective therapy,' Newsom said.
The affected counties include Los Angeles and virtually all of Southern California.
In Los Angeles, Mayor Eric Garcetti immediately implemented the shutdowns and warned that the city was 'on the verge' of raising its COVID-19 threat level from orange to red — the highest level — and resorting to shutting down all but essential businesses.
Garcetti noted that Los Angeles County now has more virus cases than Canada.
'We have never had as many people infected, or infectious,' he said. 'We've never had as many people in the hospital as there are tonight.'
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Coronavirus deaths are up 46% across the US
More than 5,000 people died from COVID-19 between July 6 and July 12, which is an increase of 46 percent compared to the previous week.
Coronavirus deaths are up 46% across the US in the last week with Texas, Arizona and Mississippi reporting the biggest weekly spikes - as 46 states continue to record new cases
By Emily Crane
Published: 09:10 EDT, 14 July 2020 | Updated: 12:32 EDT, 14 July 2020
- More than 5,000 people died from COVID-19 between July 6 and July 12, which is an increase of 46 percent compared to the previous week
- Texas, Arizona and Mississippi reported the biggest weekly spikes, according to an analysis of data
- A dozen states reported increases in deaths for at least two weeks, including California, Florida and Texas
- New cases also continue to rise with the US reporting over 400,000 infections for the week ending July 12, which was up 21 percent from the previous seven days
- Forty-six states reported more new cases of COVID-19 last week compared to the previous week
- Cases are only falling on a weekly basis in New York, Tennessee, New Jersey and Delaware
- Currently, more than 135,000 Americans have died from coronavirus and there have been more than 3.3 million infections
- Until now, the number of deaths per day from COVID-19 had been falling for months even as hot spots states like Florida, Texas and Arizona saw explosions in cases and hospitalizations
- The impact of the new surge in deaths has been felt by the healthcare workers grappling in overstretched hospitals with Texas and Arizona requesting refrigerated trucks as morgues reach capacity
Deaths related to COVID-19 have increased across the United States by 46 percent in the past week with Texas, Arizona and Mississippi reporting the biggest weekly spikes.
More than 5,000 people died from COVID-19 between July 6 and July 12, which is an increase of 46 percent compared to the previous week, according to a Reuters analysis of data from The COVID Tracking Project.
About a dozen states have reported increases in deaths for at least two straight weeks, including California, Florida and Texas.
In Texas, news deaths surged by 127 percent last week when it added 555 new deaths, bringing the total to just over 3,100.
Arizona's deaths increased by 94 percent after adding 428 deaths. The hardhit state's death toll was at 2,237 the week ending July 12.
Mississippi's deaths spike by 92 percent last week compared to the previous week. The state added 138 deaths, bringing the total to just over 1,200.
In California and Florida - two of the other hot spot states - deaths surged by more than 60 percent last week.
Florida recorded 514 deaths in the week ending July 12, bringing total to over 4,300; and California reported 686 deaths, bringing the total to 7,000. Florida on Monday added a record 132 fatalities to its death toll.
New cases also continue to rise with the US reporting over 400,000 infections for the week ending July 12, which was up 21 percent from the previous seven days.
Nationally, new COVID-19 cases have risen every week for six straight weeks.
Forty-six states reported more new cases of COVID-19 last week compared to the previous week, the analysis found.
Cases are only falling on a weekly basis in New York, Tennessee, New Jersey and Delaware.
While Southern and Western states are seeing the biggest increase in cases, infections are also rising in the Midwest with Minnesota cases up 60 percent, Missouri up 40 percent and Iowa up 30 percent.
Currently, more than 135,000 Americans have died from coronavirus and there have been more than 3.3 million infections.
Until now, the number of deaths per day from COVID-19 had been falling for months even as hot spots states like Florida, Texas and Arizona saw explosions in cases and hospitalizations.
Daily infections across the US have broken records several times in recent days.
Health officials have been warning for weeks that deaths would surge again because the fatality rate lags several weeks behind infections.
A coronavirus death, when it occurs, typically comes several weeks after a person is first infected.
Experts had predicted states that saw spikes in cases and hospitalizations would, at some point, see deaths rise too.
The impact of the new surge in deaths has been felt by the healthcare workers grappling in overstretched hospitals with Texas and Arizona requesting refrigerated trucks as morgues reach capacity.
In Arizona, capacity within intensive care units had surged to 90 percent. Hospitalizations in Texas continue to spike to record highs with more than 10,000 people being treated on Monday.
Researchers expect deaths to rise for at least several weeks but some think the count probably will not go up as dramatically as it did in the spring.
A forecast model from the University of Washington's Institute for Health Metrics is predicting the death toll to rise to 208,255 by November 1.
Experts say the death toll may not be as bad as when the pandemic first hit because testing was extremely limited early on and that many people's health behaviors have now changed with mask-wearing becoming more common in some places.
Testing for COVID-19 rose by 7.4 percent in the United States last week and set a new record high on July 10, with over 823,000 tests performed, according to the Reuters analysis.
Nationally, 8.8 percent of tests came back positive for coronavirus, up from 7.5 percent the prior week and 5 percent three weeks ago.
The World Health Organization considers a positivity rate above 5 percent to be a cause for concern because it suggests there are more cases in the community that have not yet been uncovered.
Thirty-one states had positivity test rates above 5 percent, according to the analysis, including Arizona at 27 percent, South Carolina at 19 percent and Florida at 19 percent.
The surge in new cases has prompted many states to temporarily halt the reopening of their economies or order some businesses to close for a second time.
California's Gov Gavin Newsom has once again closed bars, inside dining and, for much of the state, gyms, indoor church services and hair and nail salons in an effort to prevent COVID-19 cases from swamping hospitals.
The Gov issued the sweeping set of closures on Monday as the state recorded more than 329,000 cases and deaths topped 7,000. Hospitalizations have surged by 28 percent in the past two weeks, including a 20 percent increase in patients requiring intensive care.
'COVID-19 is not going away anytime soon, until there is a vaccine and or an effective therapy,' Newsom said.
The affected counties include Los Angeles and virtually all of Southern California.
In Los Angeles, Mayor Eric Garcetti immediately implemented the shutdowns and warned that the city was 'on the verge' of raising its COVID-19 threat level from orange to red — the highest level — and resorting to shutting down all but essential businesses.
Garcetti noted that Los Angeles County now has more virus cases than Canada.
'We have never had as many people infected, or infectious,' he said. 'We've never had as many people in the hospital as there are tonight.'
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TB Fanatic
Scratch that August trip to Hawaii. The state just extended its quarantine until Sept. 1
The state had planned to allow out-of-state travelers on Aug. 1 if they presented a negative COVID-19 test. That has been pushed back to Sept. 1.
www.usatoday.com
Scratch that August trip to Hawaii. The state just extended its quarantine until Sept. 1
Dawn Gilbertson
Published 9:14 p.m. ET July 13, 2020 | Updated 1:38 p.m. ET July 14, 2020
Hawaii delayed its plan to allow out-of-state visitors to return to the vacation hot spot by a month because of an increase in coronavirus cases in the state and on the U.S. mainland.
In late June, the governor's office announced that travelers could visit Hawaii beginning Aug. 1, no quarantine required, by presenting a negative COVID-19 test taken within 72 hours of boarding a flight. Without one, passengers arriving from the mainland would have to strictly quarantine for 14 days, a policy in place since March that has scared away most tourists and wrecked Hawaii's tourism industry. The surge in cases has made it harder for people in many states to get tested.
Hawaii Gov. David Ige said at a news conference late Monday that the travel program won't begin until Sept. 1, a decision he said was not made lightly.
"We have always said that we will make decisions based on the health and safety of our community as the highest priority," Ige said.
Monday, Hawaii reported three more coronavirus deaths and 23 new cases, bringing its total cases to 1,243. Saturday, it reported a single-day record of 42 cases, Ige said. That is a fraction of other states, thanks in part to the island state's isolation and the strict quarantine announced in March as the pandemic gripped the country.
Airline employees diagnosed: 14 Hawaiian Airlines flight attendants test positive for COVID-19 after training in Honolulu
Ige cited "uncontrolled outbreaks and surges" on the mainland as a factor in the state's decision, singling out several states with spikes, including California and Arizona, big sources of visitors to Hawaii.
"As we speak right now, the outbreaks on the mainland are not in control, and we don't believe that situation will change significantly by Aug. 1 as we had hoped," Ige said.
College students returning to school in Hawaii will be exempt from the extended quarantine, he said.
Many in Hawaii’s business community had looked forward to the testing program as it would make it easier for tourists to visit and potentially boost the economy. The quarantine requirement has virtually shut down tourism to the state. Hotels closed, and the unemployment rate stands at 22.6%, the second-highest in the nation.
Ige said he and the state’s mayors, whom he consulted, understood the gravity of the choices they had. On the one hand, he said, Hawaii could have an uncontrolled surge of COVID-19 if it reopened. On the other, delaying the traveler testing program would risk further economic damage.
“I know that this increases the burden on businesses here in the islands, especially small businesses. But we do believe that it is time to continue to protect the health and safety of our community,” Ige said at a news conference.
Hawaii is not the first state to pause or backtrack on its reopening plans. It is happening across the country as COVID-19 cases spike. Monday, California Gov. Gavin Newsom announced the statewide closure of indoor dining at restaurants and other measures. Last week, Las Vegas bars that don't serve food were shut down five weeks after reopening.
Travel restrictions are increasing, too. New York, New Jersey and Connecticut require visitors from COVID-19 hot spots to quarantine for 14 days, and Chicago added a similar measure.
Disneyland delayed its planned July 17 reopening, and Hong Kong Disneyland is closing again this week, but Disney World reopened Saturday.
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Los Angeles Reports Highest-Ever Number Of New Coronavirus Cases And Hospitalizations
L.A. County confirmed record new COVID-19 cases and hospitalizations with 4,244 new cases and and 2,103 people currently hospitalized.
deadline.com
Los Angeles Reports Highest-Ever Number Of New Coronavirus Cases And Hospitalizations
Tom Tapp
July 14, 2020 3:38pm
The day after California Governor Gavin Newsom shut down a number of business sectors in the state, the Los Angeles County Department of Public Health confirmed record new COVID-19 cases and hospitalizations in a day with 4,244 new cases and 2,103 people currently hospitalized.
That compares with 2,593 new COVID-19 cases on Monday.
Of the 2,103 people currently hospitalized, 27% of these people are confirmed cases in the ICU and 19% are confirmed cases on ventilators. According to L.A. Mayor Eric Garcetti, on Monday there were only 766 hospital beds left for the region’s 10 million residents.
That led Garcetti to say that the city’s COVID-19 threat meter is “on the border of going to red,” the highest level, which would mean a complete shutdown in L.A. owing to the pandemic.
Daily Update:
July 14, 2020
Cases: 4,244 (140,307 total)
Deaths: 73 (3,894 total)
Current Hospitalizations: 2,103 pic.twitter.com/wIV6zaYbiv
— LA Public Health (@lapublichealth) July 14, 2020
The county confirmed 73 new deaths of Covid-19. This is one of the highest number of new deaths reported in a day and may reflect a lag in the reporting of deaths over the weekend.
Testing results are available for over 1,387,000 individuals with 9% of all people testing positive.
That comes on the same day that California reports 7,346 cases, the fourth day in the past two weeks the state has seen over 7,000 new cases. Before that period, any number over 7,000 would have been a record. Test positivity rate for the state at large was 7.1 percent over a 14-day average.
Accordingly, on Monday Newsom ordered all counties to close their restaurants, movie theaters, family entertainment centers, wineries, zoos and bars for indoor service. Bars were ordered to close entirely.
Additionally, L.A. and 31 other counties on the state’s monitoring list must close fitness centers, places of worship, nail and hair salons and indoor malls. Other L.A.-local counties impacted include Santa Barbara, Ventura, San Diego, Orange and virtually every other county in Southern California.
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Amid surge, coronavirus cases in Texas break daily record again
Texas health officials on Tuesday reported a record-breaking number of new confirmed coronavirus cases in a single...
www.statesman.com
Amid surge, coronavirus cases in Texas break daily record again
Hojun Choi
Posted Jul 14, 2020 at 5:05 PM Updated Jul 14, 2020 at 7:11 PM
Texas health officials on Tuesday reported a record-breaking number of new confirmed coronavirus cases in a single day with 10,745 cases.
The previous record for the most number of newly confirmed cases in the state had been set Saturday with 10,351 cases.
The reported number of new cases had dropped significantly from 8,196 on Sunday to 5,655 on Monday.
Health officials said the current estimate for active COVID-19 cases in Texas is at 129,338. The total estimated number of recoveries is at 142,398, according to officials.
Health officials also said 87 more people had died in Texas from coronavirus-related causes.
A total of 3,322 people have died in the state from the coronavirus to date, according to the Texas Department of State Health Services.
Harris County has the state’s highest number of deaths with 466 fatalities reported, followed by Dallas County with 457 and Tarrant County with 272.
State health officials on Tuesday said 10,569 people remain hospitalized because of the coronavirus. The number of hospitalizations had surpassed 10,000 for the first time on Friday.
On Monday, Gov. Greg Abbott announced that the U.S. Defense Department will aid the state’s efforts to combat COVID-19 by providing additional medical task force teams.
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Illinois Averaged More Than 1,000 New Coronavirus Cases a Day Over Last 7 Days
For the first time in more than a month, the state of Illinois has averaged more than 1,000 new coronavirus cases a day over the last seven days. According to data released by the Illinois Department of Public Health, the state’s rolling seven-day average of new COVID-19 cases stands at 1,007.7...
www.nbcchicago.com
Illinois Averaged More Than 1,000 New Coronavirus Cases a Day Over Last 7 Days
Published July 14, 2020 • Updated on July 14, 2020 at 5:27 pm
For the first time in more than a month, the state of Illinois has averaged more than 1,000 new coronavirus cases a day over the last seven days.
According to data released by the Illinois Department of Public Health, the state’s rolling seven-day average of new COVID-19 cases stands at 1,007.7 cases per day. The last time the number was over the 1,000 mark was on June 8, when the state was at 1,025.9 new coronavirus cases per day.
That number has been on the rise since June 18, when the state hit a low water mark of 4,175 cases reported over a seven day span.
While the increase could be tied at least in part to the state’s loosening of restrictions, increased testing has also caused that number to trend upward. When Illinois last registered an average of 1,000 new cases per day over a seven-day stretch, the state had conducted 140,600 cases during that time period.
As of today, Illinois has reported 231,606 tests over the last seven days, the highest-level of testing conducted in the state since the pandemic began.
That increase in testing has also led to a decline in the state’s seven day positivity rate on tests. On June 8, Illinois’ seven day positivity rate was at 5.1 percent. As of today, that number is just over 3 percent.
Even still, the increase in positive cases is worth noting, as other states across the country have seen dramatic increases in cases over the summer. Illinois, as one of the last states to begin loosening COVID-19 restrictions, has seen increases in positive tests, but not to the extent that states such as Florida, Texas and California have.
The state’s Southern Region has seen case numbers and positivity rates increasing in the last week or so, with a positivity rate of 7 percent each of the last three days.
That increase in positive tests has pushed the region’s positivity rate up to five percent, more than double what it had been 14 days ago.
Meanwhile, the Northeast Region, where most of the state’s coronavirus cases had come from early in the pandemic, has remained largely flat in positivity rate, according to data from the IDPH.
Illinois Gov. J.B. Pritzker has thus far declined to impose travel restrictions on the state, but Chicago Mayor Lori Lightfoot’s administration has said that all travelers from coronavirus hotspots will need to self-quarantine for 14 days after arriving in the city.
Pritzker did say this week that he would consider closing indoor service in restaurants and bars, among other restrictions, if coronavirus numbers continue to rise.
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