Coronavirus Update

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Coronavirus Update 1-27

Recent Developments

January 27, 2021

“There is nothing we can do to change the trajectory of the pandemic in the coming months.” 

President Biden

“I believe President Biden made it very clear, the plane is in a nosedive, and we gotta pull it up. And you’re not going to do that overnight. But we’re gonna pull it up, we have to pull it up. Failure is not an option here, and so we will.”   

Health and Human Services Secretary-designate Xavier Becerra, walking back President Biden’s comments

“We need to assume now what has been circulating in the UK does have an increase in virulence, meaning the power of the virus to cause more damage, including death.”  

Dr. Fauci

“It’s critical to understand where the virus is, where it’s increasing, where it’s decreasing and react to the slightest uptick.  We’re still slow in reaction and I think because in the early days we were so focused on flattening the curves and preserving the hospitals that people think if the hospitals are okay then we’re doing okay. But we need to react when you see that tiniest little uptick in test positivity.”   

Dr. Deborah Brix

“If you have a physical covering with one layer, you put another layer on, it just makes common sense that it likely would be more effective.”  

Dr. Fauci

Index

Navigational Tips:  Except for the stories listed under Linked Stories, all of the stories listed below are included in this update.  And to the extent available, we have embedded links in the title of the stories to the extent available so that you can quickly jump to the original story on the internet if you want by clicking on the title.  If you reading the Word document, you can jump to a section by holding down the control key+clicking on the title of the section.

Highlighted stories includes information we found interesting.  An (!) indicates a story that includes new, promising/breakthrough or unexpected/surprising information.  A (*) indicates information that may be useful in connection with your plans and preparations regarding the coronavirus and C19.  And © indicates that a story contains information that may contradict or be inconsistent with other information.

A. Pandemic Headlines

B. Numbers & Trends

  1. Cases & Tests
  2. Deaths
  3. Top 5 States in Cases, Deaths, Hospitalizations, ICU Patients & Positivity
  4. US Trends

C. New Variants (Mutations) of Coronavirus

  1. Emerging Variants & Mortality  (!)
  2. Studies of South African Coronavirus Strain Raise Concerns About Immune Response  (!)
  3. We could know soon whether vaccines work against the South African variant 
  4. California may have highly contagious homegrown C19 strain

D. New Scientific Findings & Research

  1. People With High Omega-3 Blood Levels Less Likely to Die From C19  (!) (*)
  2. C19 Virus Needs Cholesterol to Invade Cells – What This Means for People Taking Statins  (!) (*)
  3. New Research Shows We May Already Have Some Degree of Pre-existing C19 Immunity
  4. Big Differences in Long-Term Immunity Resulting From Mild vs. Severe C19 Cases  (!) (*)
  5. NSAIDs – Such As Advil and Meloxicam – Might Exacerbate or Suppress C19 Depending on Timing  (!) (*) ©
  6. The immune system mounts a lasting defense after recovery from C19  (!) ©

E. Vaccines & Testing

  1. Vaccine Development & Efficacy
  2. Vaccines versus the variants  (!)

F. Improved & Potential Treatments

  1. Regeneron says antibody cocktail is 100% effective in preventing symptomatic C19 infection  (!)
  2. Colchicine, a gout drug, shows preliminary promise for C19
  3. Lilly Antibody Drug Prevents C19 in Nursing Homes 
  4. New C19 therapy could be ’30 times more potent than Remdesivir’  (!)
  5. Nasal spray that blocks C19 could be available by summer  (!)
  6. In preclinical models, antiviral inhibits C19 better than Remdesivir     

G. Concerns & Unknowns

  1. Rogue antibodies could be driving severe C19  (!)
  2. Patients in cancer remission at high risk for severe C19 illness  (*)
  3. Covid linked to risk of mental illness and brain disorder  (!)
  4. Examining Infection Fatality Rates: C19 Is Dangerous for Middle-Aged Adults, Not Just the Elderly 
  5. C19 virus helps block host immunity 
  6. Lifetime smoking history associated with C19 severity

H. Back to School!?

  1. CDC officials say most available evidence indicates schools can be safe if precautions are taken on campus and in the community
  2. What new COVID variants mean for schools is not yet clear  

I. Innovation & Technology

  1. Researchers are developing color-changing stickers to detect C19(!)

J. Projections & Our (Possible) Future

  1. New C19 Model Shows Little Benefit in Vaccinating High-Risk Individuals First  ©
  2. C19 model reveals key role for innate immunity in controlling viral load

K. Lockdowns

  1. Another Study Shows—Yet Again—That Lockdowns Don’t Work

L. Practical Tips & Other Useful Information

  1. Depression and Stress Could Dampen Efficacy of C19 Vaccines: Interventions Could Boost Immunity  (*)
  2. Which masks are the most effective against new C19 strain?  (*)
  3. You Tested Positive for C19. Now What?  (*)

M. Johns Hopkins COVID-19 Update

N. Linked Stories

  1. Most Lungs Recover Well After C19
  2. Covid lockdown loneliness linked to more depressive symptoms in older adults
  3. PTSD link to pandemic panic
  4. For some, GI tract may be vulnerable to C19 infection
  5. WHO issues new clinical advice on treating C19 patients
  6. Novel molecules to combat asthma and covid-related lung diseases discovered
  7. Continued strict control measures needed to reduce new C19 strains
  8. C19 Warnings Were on Twitter Well Before the Official Outbreak of the Pandemic
  9. Obesity, Impaired Metabolic Health and C19: The Interconnection of Global Pandemics
  10. New Results From Monkeys Suggest C19 Vaccines Will Be Successful
  11. Century of Data Shows C19 Likely to Impact the Brain Long-Term
  12. Microwaves used to deactivate coronavirus, flu, other aerosolized viruses
  13. Nearly one in four families hesitant to take their child to ER during C19 pandemic
  14. Coronavirus reacts to antibodies of virus from 2003 SARS outbreak
  15. C19 infection in immunodeficient patient cured by infusing convalescent plasma
  16. Many junior doctors feel out of their depth with the end-of-life decisions faced during C19 pandemic
  17. OHIO researchers ID potential target for anti-viral drugs to battle COVID 
  18. New trial finds arthritis drug no better than standard care for severe C19
  19. Experts weigh economic impact as world nears 100 million C19 cases
  20. Why did the world’s pandemic warning system fail when COVID hit?

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A. Pandemic Headlines

(In no particular order)

B. Numbers & Trends

Note: Unless otherwise noted, (i) all cases/deaths are confirmed cases/deaths that have been reported, (ii) all numbers reported in this update are as of the end of the most recent reporting period, and (iii) all changes reflect changes since the preceding day.  

Sources: https://www.worldometers.info/coronavirus/ and https://covidtracking.com/

1.      Cases & Tests

Worldwide Cases:  
  • Total Cases = 10,812,620
  • New Cases (7 day average) = 585,285
Observations:
  • 7 day average of new cases has been declining at a rapid rate since 1/11
  • Since 1/11, the 7 day average has declined from 743,312 to 585,285, a decrease of 21.3%
US Cases:
  • Total Cases = 26,001,222
  • New Cases (7 day average) = 171,270
  • Percentage of New Global Cases = 29.3%
Observations:
  • 7 day average of new cases has been declining at a rapid rate since 1/11
  • Since 1/11, the 7 day average has declined from 254,214 to 171,270, a decrease of 32.6%

2.      Deaths

  • Worldwide Deaths:
  • Total Deaths = 2,165,190
  • New Deaths (7 day average) = 14,318
Observations:
  • Record high 7 day average of new deaths
  • Although the 7 day average has been increasing since 12/28, the rate of growth started slowing on 7/12
US Deaths:
  • Total Deaths = 435,452
  • New Deaths (7 day average) = 3,417
  • Percentage of Global New Deaths = 23.9%
Observations:
  • 7 day average of new deaths is slightly below record high of 3,421 on 1/16
  • Although the 7 day average began to decline on 1/16, it began to increase rapidly on 1/20

3.  Top 5 States in Cases, Deaths, Hospitalizations, ICU Patients & Positivity (1/26) 

Key Observations
  • The US Positivity Rate fell to its lowest level since 10/16
  • Hospitalizations fell 12.0% last week and reached the lowest level since 12/12
  • Patients in ICU fell 10.7% last week and reached the lowest level since 12/8
Positivity Trends
  • The US Positivity Rate fell to 11.2% on 1/24, the lowest level since 11/11/20. The Rate increased slightly to 11.3% on 1/26. For the first time since 10/16/20, all 50 states have positivity rates below 40%.
    • Despite the decline in US Positivity, thirteen states reported higher positivity rates over the last week (+9 states since 1/19).
    • ND leads the US with an average of 35% of all tests resulting positive
    • Zero states: 7-day positivity rates greater than 40% (-3 since 1/19)
    • Eight states: 7-day positivity rates greater than 30% (unch since 1/19)
    • Sixteen states: 7-day positivity rates greater than 20% (+5 since 1/19)
    • Four states (MS, AK, OR, IL): 7-day positivity rates less than 5% (+1 since 1/19)
    • In total, 46 states have 7-day positivity rates greater than 5% (-1 since 1/19)
Hospitalization Trends
  • Hospitalizations declined 12.0% last week to 108,957 patients. This represents the lowest level since 12/12/20. 
    • Three states had increases of hospitalized patients of more than 10% in the past week. (+1 since 1/19)
    • 27 states have more than 1,000 hospitalized patients (-1 since 1/19).
    • 46 states saw decreases in the number of hospitalized patients over the past week. (+1 since 1/19).
Patients in ICU Trends
  • The number of patients in the ICU declined 10.7% last week to 20,573 patients. This represents the lowest level since 12/8/20.
    • Three states have seen the number of ICU patients increase by more than 10% since a week ago (-1 since 1/19).
    • 28 states have more than 100 patients in ICU, (-1 since 1/19).
    • 45 states saw decreases in the number of ICU patients over the past week (+16 since 1/19).

4.      US Trends

  • It is becoming more clear that the US has passed a peak in terms of daily incidence, and the current average is less than what it was prior to the Thanksgiving holiday weekend. In light of fluctuations in reporting over the winter holidays, it is difficult to determine when the daily incidence actually peaked; however, the peak in terms of reported incidence was 248,706 new cases per day on January 8. In addition to daily incidence, we are beginning to observe an associated decrease in hospitalizations at the national level.
  • This trend is evident at the regional and state levels as well. All 4 regions have reported decreasing daily incidence since approximately January 8-10, including a further decrease in the Midwest, which has reported a steady decline in daily incidence since mid-to-late November. According to data from the COVID Exit Strategy website, 28 states are reporting decreasing daily incidence over the past 2 weeks, including nearly every state stretching from the Midwest to the Pacific Northwest as well as several states in the South, Mid-Atlantic, and Northeast.
  • According to data from The COVID Tracking Project, 45 states (plus Washington, DC) are reporting decreasing daily incidence over the past week, and 5 are holding steady (-10% to +10%). In fact, only Tennessee is reporting increased incidence over the past week, but at +7%, it still falls under the category of “Staying the Same.” Similarly, hospitalizations are decreasing in all 4 regions. Additionally, 33 states are reporting decreasing hospitalizations over the past week, and 15 (plus Washington, DC) are reporting steady hospitalizations (-10% to +10%)—compared to only 2 states reporting increases.
  • Looking at mortality at the regional level, C19 deaths continue to decrease steadily in the Midwest, and the Northeast region appears to have recently passed a peak. The South and West regions may be at or approaching their own peaks, but holiday-related delays in reporting make it difficult to determine the longer-term trend in these regions. At the state level, 21 states (plus Washington, DC) are reporting decreasing daily mortality over the past week, compared to 11 with increasing mortality and 18 holding relatively steady (-10% to +10%).
  • The US has now administered more than half of the distributed vaccine doses. The US CDC reported 41.42 million vaccine doses distributed and 22.73 million doses administered (54.9%%), including 2.71 million administered in long-term care facilities (LTCFs). In total, 19.25 million people have received at least 1 dose of the vaccine, and 3.35 million have received both doses. The US is now averaging 1.13 million doses administered per day, an increase of 35% compared to this time last week. The breakdown of doses by manufacturer remains relatively even, with slightly more Pfizer/BioNTech doses administered (12.55 million; 55%) than Moderna (10.08 million; 45%).
  • The Johns Hopkins CSSE dashboard reported 25.34 million US cases and 422,583 deaths as of 1:30pm EST on January 26.

Source:      Johns Hopkins COVID-19 Update

C. New Variants (Mutations) of Coronavirus

1.      Emerging Variants & Mortality 

  • New evidence indicates the UK variant (B.1.1.7) of concern (VOC) may be associated with increased mortality compared to other strains of the coronavirus (SARS-CoV-2).
  • At a press conference this week, Sir Patrick Vallance, the UK’s Government Chief Scientific Advisor, said that infection with the new variant may be associated with an increased risk of death, in addition to its increased transmissibility. He noted that the mortality risk could be on the order of 30-40% higher for some individuals, but he also said that further analysis is needed to better characterize this relationship.
  • Analysis published by the UK’s New and Emerging Respiratory Virus Threats Advisory Group (NERVTAG) found that that mortality risk was significantly higher in individuals infected with the B.1.1.7 variant across multiple age groups, with increases ranging from 29% to 91% in multiple studies.
  • In response to the potential for increased mortality, UK Prime Minister Boris Johnson called for redoubled vigilance and adherence to C19 prevention measures in order to protect the capacity of national healthcare system. Fortunately, current vaccine candidates still appear to be effective against the variant. The UK government will continue to drive toward its goal of vaccinating 15 million people by mid-February in order to protect the most vulnerable against infection by any variant of SARS-CoV-2. 
  • In the US, Dr. Anthony Fauci acknowledged the NERVTAG results as highly concerning and in need of further study in the coming weeks. He emphasized that current vaccines still appear to be effective against existing VOCs, but adjustments can and will be made as needed.
  • Dr. Fauci did note that monoclonal antibody treatments did appear to be significantly less effective against some VOCs compared to reference strains.

Source:      Johns Hopkins COVID-19 Update

2.      Studies of South African Coronavirus Strain Raise Concerns About Immune Response

  • ●      Three new laboratory studies are raising concerns that the immune response triggered by a C19 infection or vaccination may be less effective at protecting against the new strain of the coronavirus that first emerged in South Africa.
  • A fourth study, conducted by scientists at BioNTech SE and Pfizer Inc. and published by the companies, showed that their vaccine successfully neutralized a variant that was initially detected in the U.K. That study didn’t include the South African strain.
  • More than a year into the pandemic, the discovery of new variants that appear to have made the virus more contagious is forcing researchers to adapt their understanding of the coronavirus that causes C19. One concern, researchers said, is that the new strains are emerging in countries where a significant percentage of people have already built up an immune response to earlier variants after getting C19.
  • Studies on lab-grown viruses and blood drawn from people who have either recovered from a previous bout of C19 or received a C19 vaccine are some of the first experiments scientists conduct when they want to find out more about a new variant. Researchers who worked on the studies said that the tests only examined the response of certain antibodies, while the human immune system also includes so-called T-cells, blood cells that help attack the virus, and other types of cells.
  • More definitive data will come from human trials of C19 vaccines under way in South Africa and in the U.K. and whose results are expected within weeks. Those results will give a better indication of how vaccines perform against the new strains.
  • For two of the studies, researchers in South Africa tested how the new variant, which has driven a powerful second wave of infections in the country, responded to blood drawn from people who had C19 in the first wave, when other versions of the virus were circulating. What they found was that the new variant was either entirely resistant to antibodies generated from an earlier infection or the antibodies were significantly less able to neutralize the virus.
  • A second study replicated the South African variant’s spike protein, through which the virus attaches to and infects human cells, on a different virus. New C19 vaccines—including those developed by BioNTech and Pfizer and by Moderna Inc. —also target the coronavirus’s spike protein.
  • That study found that blood from 21 of 44 people who had previously had C19 failed to neutralize the virus. Only three blood samples—from people who had suffered very severe cases of C19—were able to mount a powerful attack.
  • The findings may mean that variants such as the South African one could infect people for a second time “and may foreshadow reduced efficacy of current spike-based vaccines,” the study concluded.
  • A third study—conducted by researchers at Rockefeller University in New York and the California Institute of Technology in Pasadena—ran a similar set of tests as the South African scientists, but using blood drawn from people who had received either the Pfizer or Moderna shots.
  • That study found that three prominent mutations in the South African variant reduced the ability of vaccine-generated antibodies to neutralize the virus by a small but significant margin.
  • One possible reason for the difference in results from the three studies is that the U.S. scientists only looked at mutations in one part of the spike protein, known as the receptor-binding domain, that latches onto human cells. In the two studies done in South Africa, some of the biggest impact on antibody response came from another part of the spike protein, known as the N-Terminal, which is also a target for neutralizing antibodies and whose significance scientists are only starting to understand.

Source:      https://www.wsj.com/articles/studies-of-south-african-coronavirus-strain-raise-concerns-about-immune-response-11611311401

3.      We could know soon whether vaccines work against the South African variant

  • The rise in cases in South Africa has been linked to a new, highly mutated form of the C19 virus. And it’s just part of a wider pattern being seen around the world. Over the last month, weary researchers racing to understand new variants in Africa, Brazil, and the United Kingdom have pumped out a series of alarming reports on preprint servers, websites, and in official reports, describing a coronavirus that is changing in ways that appear to let it shrug off lockdowns, avoid antibodies, and retake cities, like London or Manaus, that already suffered through big first waves.
  • Indeed, in a few short weeks the perception among some scientists of the coronavirus has gone from a static, slow-changing virus that’s easily walloped by vaccine technology to something more like a terrorist shapeshifter that could put a decisive end to the pandemic out of sight.
Will vaccines still work?
  • Most of the world’s attention has been on a so-called British variant of the covid virus; it seems to spread faster than the original version and has appeared in dozens of countries, including the US. On Friday, January 22, the UK prime minister, Boris Johnson, said government advisers warned this strain may also be more deadly, killing the infected about 30% more often.
  • Faster spreading, more deadly, versions of the coronavirus can still be dealt with using masks and social distancing. But the variant in South Africa, called 501Y.V2 and first described by gene sleuths on December 22, not only spreads faster but, alarmingly, also appears to evade antibodies from the blood of people previously infected by C19, and, in theory, could also lessen the effect of vaccines, society’s main hope of curbing the global outbreak.
  • Such lab evidence of “immune escape” makes the variant in South Africa “much more concerning” than the one in the UK, according to Anthony Fauci, director of the US National Institute of Allergy and Infectious Diseases, speaking at his first press conference under the new Biden administration on January 21.  “The real question that people are quite clearly interested in is: What is the impact on the vaccine?” Fauci said.
  • What Fauci didn’t mention is that we could have a real-world answer to that question as soon as next week thanks to a large vaccine trial that recruited thousands of South Africans between September and December, just as the dangerous variant spread widely.
  • That vaccine, from Johnson and Johnson, has been widely anticipated because it’s given as a single shot and is easily stored, making it easier to get into arms than the super-cooled, two-dose messenger RNA vaccines from Moderna and Pfizer authorized in the US last month.
  • Now, though, the J&J trial may unexpectedly answer the big question of whether vaccines will protect against the 501Y.V2 variant in South Africa or not. That could be determined if data show the shot is less effective in South Africa than it has been in the US, where part of the trial occurred.
  • “It will be wonderful if it has equal efficacy against the South Africa strain. If it doesn’t, that is telling us something,” says Lawrence Corey, a virologist at Fred Hutchinson Cancer Research Center in Seattle, who leads the operations center for the C19 Prevention Network, which coordinates vaccine trials financed by the US government.

Source:      https://www.technologyreview.com/2021/01/23/1016684/whether-jnj-vaccine-works-against-scary-south-african-coronavirus-variant/

4.      California may have highly contagious homegrown C19 strain

  • Scientists in California believe there is a homegrown coronavirus strain in the state that could be responsible for the dramatic rise in cases, a report said Sunday.
  • Two separate research groups have discovered the apparent California strain while looking for the new variant that is believed to have come from the United Kingdom, according to the Los Angeles Times.
  • The supposed California strain is in the same “family tree” as the UK strain and could be behind the state’s spread over the past few months, the paper said.
  • One of the labs that discovered the strain, Cedars-Sinai Medical Center in Los Angeles, said it amounted to 24% of about 4,500 viral samples gathered throughout California in the last weeks of 2020.
  • Another analysis found that 25% of 332 samples taken in Northern California were of the new strain.
  • “There was a homegrown variant under our noses,” Dr. Charles Chiu, a laboratory medicine specialist at University of California, San Francisco, told the newspaper.
  • Chiu said they only found the strain when searching for the UK variant.

Source:      https://nypost.com/2021/01/25/california-may-have-highly-contagious-homegrown-covid-19-strain/

D.      New Scientific Findings & Research

1.      People With High Omega-3 Blood Levels Less Likely to Die From C19 

  • Researchers with the Fatty Acid Research Institute (FARI) and collaborators at Cedars-Sinai Medical Center in Los Angeles and in Orange County, CA, have published the first direct evidence that higher omega-3 blood levels may reduce risk for death from C19 infection. The report was published in the journal Prostaglandins, Leukotrienes and Essential Fatty Acids on January 20, 2021.
  • There are several papers in the medical literature hypothesizing that omega-3 fatty acids should have beneficial effects in patients with C19 infection, but up until now, there have been no published peer-reviewed studies supporting that hypothesis.
  • This study included 100 patients admitted to the hospital with C19 for whom admission blood samples had been stored. Clinical outcomes for these patients were obtained and blood was analyzed for the Omega-3 Index (O3I, red blood cell membrane EPA+DHA levels) at OmegaQuant Analytics (Sioux Falls, SD). Fourteen of the patients died.
  • “While not meeting standard statistical significance thresholds, this pilot study – along with multiple lines of evidence regarding the anti-inflammatory effects of EPA and DHA – strongly suggests that these nutritionally available marine fatty acids may help reduce risk for adverse outcomes in C19 patients. Larger studies are clearly needed to confirm these preliminary findings,” said Arash Asher, MD, the lead author on this study.
  • Agreeing with Dr. Asher, cardiology researcher and co-developer with Dr. Harris of the Omega-3 Index, Clemens von Schacky, MD, (CEO, Omegametrix GmbH, Martinsried, Germany, and not involved with the study) said, “Asher et al have demonstrated that a low Omega-3 Index might be a powerful predictor for death from C19. Although encouraging, their findings clearly need to be replicated.”
  • Omega-3 expert James H. O’Keefe, Jr., MD, (Director of Preventive Cardiology, Saint Luke’s Mid America Heart Institute, Kansas City, MO, and also not involved with the study) observed, “An excessive inflammatory response, referred to as a ‘cytokine storm,’ is a fundamental mediator of severe C19 illness. Omega-3 fatty acids (DHA and EPA) have potent anti-inflammatory activities, and this pilot study provides suggestive evidence that these fatty acids may dampen C19’s cytokine storm.”

Source:      https://scitechdaily.com/people-with-high-omega-3-blood-levels-less-likely-to-die-from-covid-19/

2.      C19 Virus Needs Cholesterol to Invade Cells – What This Means for People Taking Statins

Researchers engineered cells to carry either a protein (green) from SARS-CoV-2 or its human target ACE2 (magenta). When near each other, the cells’ membranes fused. Researchers think a similar process lets the virus slip into cells.

  • People taking cholesterol-lowering drugs may fare better than others if they catch the novel coronavirus. A new study hints at why: the virus relies on the fatty molecule to get past the cell’s protective membrane.
  • To cause C19, the coronavirus (SARS-CoV-2) must force its way into people’s cells – and it needs an accomplice. Cholesterol, the waxy compound better known for clogging arteries, helps the virus open cells up and slip inside, Howard Hughes Medical Institute Investigator Clifford Brangwynne’s lab reports.
  • Without cholesterol, the virus cannot sneak past a cell’s protective barrier and cause infection, the team writes in a preprint posted to bioRxiv. The work, which recreated the early stage of infection in lab-grown cells, has not yet undergone the scientific vetting process of peer review.
  • “Cholesterol is an integral part of the membranes that surround cells and some viruses, including SARS-CoV-2. It makes sense that it should be so important for infection,” says Brangwynne, a biophysical engineer at Princeton University.
  • The finding might underlie the better health outcomes seen in C19 patients taking cholesterol-lowering drugs known as statins, he adds. Although scientists haven’t yet established the mechanism responsible, this study and another published last fall suggest the drugs prevent SARS-CoV-2 from getting into cells by denying it cholesterol.
  • This discovery of cholesterol’s importance could help scientists develop new stopgap measures to treat C19 until most people are vaccinated, Brangwynne says. The work may also shed light on a strange feature of the disease: the formation of giant, compound cells found in the lungs of C19 patients. In their experiments, the scientists saw similar mega cells emerge under the microscope. 
Mimicking a viral infection
  • In the lab, the researchers watched as lab-grown cells with these proteins interacted. First, tiny tentacles emerged from cells with ACE2 and stuck to spike proteins on nearby cells. At these points, the two cellular membranes fused and openings formed, letting the cells’ contents mix. Eventually, the two cells melded together – similar to how scientists expect the virus merges with a cell to infect it.
  • The researchers, including Princeton’s David Sanders, Chanelle Jumper, and Paul Ackerman, tried to disrupt this cell melding. Using an automated system, they tested the effects of about 6,000 compounds, as well as more than 30 tweaks to the spike protein. These experiments and others suggested that if SARS-CoV-2’s membrane lacks cholesterol, the virus cannot enter its target cell.
  • This isn’t the first evidence implicating cholesterol. The previous study, by a group at the University of California, San Diego, found that the body’s immune response to the virus produces a compound that depletes cholesterol – but in this case from the cell’s own membrane, not the virus’s.
  • “Cholesterol has been very well studied as an important factor in a large number of viral infections,” says Peter Kasson, a scientist at the University of Virginia who studies the physical mechanisms of viral disease. “The interesting thing is that cholesterol’s role in viral entry varies a lot between viruses.” It’s not clear exactly how cholesterol aids SARS-CoV-2, but understanding that process could offer clues about the biology of infection, says Kasson, who was not involved in the research.
  • The apparent beneficial effect of statins extends to other viral infections, too. Some research suggests that these drugs impair the influenza virus by depriving it of cholesterol, Kasson says. But that may not be the only way the drugs can alter the course of viral infections, he says. “It’s a little complicated because statins also modify the immune response.”
Mysterious mega cells
  • As Brangwynne’s experiments ran, his team noticed something strange. The cells continued to engulf one another, spilling their contents together like eggs cracked into a bowl. The compound cells, known as syncytia, that appeared under the microscope resemble those found in healthy tissues, such as muscle and the placenta, and in some viral diseases.

Many cells can fuse together, producing mega cells (green), or syncytia, similar to those found in the lungs of C19 patients.

  • “People already knew that the C19 virus will create syncytia, but the researchers were able to visualize the process beautifully,” says Jennifer Lippincott-Schwartz, a senior group leader at HHMI’s Janelia Research Campus, who was not involved in the research. “Cell-cell fusion is itself a really under-studied area in biology.”
  • The experiments likely illustrate how mega cells found in patients’ lungs form, she says. “The formation of syncytia can be very injurious in the case of COVID, where it can destroy lung tissues and lead to death.”
  • Brangwynne says it’s not clear yet whether or not syncytia play a major role in the progression of C19. But, his team writes, the discovery of cholesterol’s contribution could help scientists fight the disease. “Our findings underscore the potential utility of statins and other [similar] treatments.”

Source:      https://scitechdaily.com/covid-19-virus-needs-cholesterol-to-invade-cells-what-this-means-for-people-taking-statins/

3.      New Research Shows We May Already Have Some Degree of Pre-existing C19 Immunity 

  • The results of a study led by Northern Arizona University and the Translational Genomics Research Institute (TGen), an affiliate of City of Hope, suggest the immune systems of people infected with C19 may rely on antibodies created during infections from earlier coronaviruses to help fight the disease.
  • C19 isn’t humanity’s first encounter with a coronavirus, so named because of the corona, or crown-like, protein spikes on their surface. Before SARS-CoV-2 — the virus that causes C19 — humans have navigated at least 6 other types of coronaviruses.
  • The study sought to understand how coronaviruses (CoVs) ignite the human immune system and conduct a deeper dive on the inner workings of the antibody response. The published findings, “Epitope-resolved profiling of the SARS-CoV-2 antibody response identifies cross-reactivity with endemic human coronaviruses,” were published on January 19, 2021, in the journal Cell Reports Medicine.
  • “Our results suggest that the C19 virus may awaken an antibody response that existed in humans prior to our current pandemic, meaning that we might already have some degree of pre-existing immunity to this virus.” said John Altin, an assistant professor in TGen’s infectious disease branch and the study’s senior author.
  • This knowledge could help researchers design new diagnostics, evaluate the healing powers of convalescent plasma, develop new therapeutic treatments and — importantly — help design future vaccines or monoclonal antibody therapies capable of protecting against mutations that may occur in the C19 virus.
  • By comparing patterns of reactivity against different coronaviruses, the researchers demonstrated that SARS-CoV-2 could summon immune system antibodies originally generated in response to past coronavirus infections. This cross-reactivity occurred at two sites in the SARS-CoV-2 Spike protein; the protein on the surface of virus particles that attaches to ACE2 proteins on human cells to facilitate cell entry and infection.
  • “Our findings highlight sites at which the SARS-CoV-2 response appears to be shaped by previous coronavirus exposures, and which have potential to raise broadly-neutralizing antibodies. We further demonstrate that these cross-reactive antibodies preferentially bind to endemic coronavirus peptides, suggesting that the response to SARS-CoV-2 at these regions may be constrained by previous coronavirus exposure,” said Altin, adding that more research is needed to understand the implications of these findings.
  • The findings could help explain the widely varying reactions C19 patients have to the disease; from mild to no symptoms, to severe infections requiring hospitalization, and often resulting in death. It’s also possible that differences in the pre-existing antibody response identified by this study could help to explain some of the difference in how severely C19 disease manifests in old versus young people, who will have different histories of infections with the common coronaviruses.
  • “Our findings raise the possibility that the nature of an individual’s antibody response to prior endemic coronavirus infection may impact the course of C19 disease,” Ladner said.

Source:      https://scitechdaily.com/new-research-shows-we-may-already-have-some-degree-of-pre-existing-covid-19-immunity/

4.      Big Differences in Long-Term Immunity Resulting From Mild vs. Severe C19 Cases 

  • A big question on people’s minds these days: how long does immunity to SARS-CoV-2 last following infection?
  • Now a research team from La Jolla Institute for Immunology (LJI), The University of Liverpool and the University of Southampton has uncovered an interesting clue. Their new study suggests that people with severe C19 cases may be left with more of the protective “memory” T cells needed to fight reinfection.
  • “The data from this study suggest people with severe C19 cases may have stronger long-term immunity,” says study co-leader LJI Professor Pandurangan Vijayanand, M.D., Ph.D.
  • The research, published on January 21, 2021, in Science Immunology, is the first to describe the T cells that fight SARS-CoV-2 in “high resolution” detail.
  • “This study highlights the enormous variability in how human beings react to a viral challenge,” adds co-leader Christian H Ottensmeier, M.D., Ph.D., FRCP, a professor at the University of Liverpool and adjunct professor at LJI.
  • Since early in the C19 pandemic, scientists at LJI have investigated which antibodies and T cells are important for fighting SARS-CoV-2. As experts in genomics, Vijayanand and Ottensmeier have used sequencing tools to uncover which T cell subsets may control disease severity. In October, the team published the first detailed look at how CD4+ T cells respond to the virus.
  • To the researchers’ surprise, they saw weaker CD8+ T cell responses in patients with milder C19 cases. The researchers saw the strongest CD8+ T cell responses in the severely ill patients who required hospitalization or ICU support.
  • “There is an inverse link between how poorly T cells work and how bad the infection is,” says Ottensmeier. “I think that was quite unexpected.”
  • One could expect to see a stronger CD8+ T cell response in the mild cases, since these are the cases where the immune system was equipped to fight off a severe infection — but the study showed the opposite. In fact, CD8+ T cells in the milder cases showed the molecular signs of a phenomenon called T cell “exhaustion.” In cases of T cell exhaustion, cells receive so much immune system stimulation during a viral attack that they are less effective in doing their jobs.
  • While more research is needed, Vijayanand and Ottensmeier think it is worth studying whether T cell exhaustion in the mild C19 cases may hinder a person’s ability to build long-term immunity.
  • “People who have severe disease are likely to end up with a good number of memory cells,” says Vijayanand. “People with milder disease have memory cells, but they seem exhausted and dysfunctional — so they might not be effective for long enough.”
  • The new study provides a valuable window into CD8+ T cell responses, but it is limited because it relies on the CD8+ T cells found in blood samples. As a next step, the researchers hope to shed light on how T cells in tissues hit hardest by SARS-CoV-2, such as the lungs, react to the virus. This step will be important because the memory T cells that provide long-term immunity need to live in the tissues.

Source:      https://scitechdaily.com/big-differences-in-long-term-immunity-resulting-from-mild-vs-severe-covid-19-cases/

5.      NSAIDs – Such As Advil and Meloxicam – Might Exacerbate or Suppress C19 Depending on Timing 

  • New research shows that non-steroidal anti-inflammatory drugs (NSAIDs) reduced both antibody and inflammatory responses to the coronavirus (SARS-CoV-2) infection in mice. The study appears this week in the Journal of Virology, a publication of the American Society for Microbiology.
  • The research is important because “NSAIDs are arguably the most commonly used anti-inflammatory medications,” said principal investigator Craig B. Wilen, Assistant Professor of Laboratory Medicine and Immunology, Yale University School of Medicine.
  • In addition to taking NSAIDs for chronic conditions such as arthritis, people take them “for shorter periods of time during infections, and [during] acute inflammation as experienced with C19, and for side effects from vaccination, such as soreness, fever, and malaise,” said Dr. Wilen. “Our work suggests that the NSAID meloxicam dampens the immune response to SARS-CoV-2 infection.”
  • The research also suggests that the consequences of NSAID use during natural infection and vaccination should be evaluated in humans, said Dr. Wilen. “This data likely exists, particularly in the clinical trials for the vaccines, so it should be mined to see if it produces antibody responses in people.”
  • “Taking NSAIDs during C19 could be harmful or beneficial, depending on the timing of administration,” said Dr.Wilen. The potent anti-inflammatory, dexamethasone (not an NSAID), is detrimental to C19 sufferers when taken early in the infection, but beneficial when administered during later stages of C19, said Dr. Wilen.
  • Similarly, NSAIDs’ anti-inflammatory activity might be detrimental early in SARS-CoV-2 infection, because at this stage, inflammation is usually helpful. That changes at later stages of C19, particularly if the patient undergoes an intense inflammation known as a cytokine storm. A cytokine storm is an immune response of inflammatory compounds that often occurs in C19 patients, can lead to complications, need for the intensive care unit, and even death.
  • A reduction in neutralizing antibodies caused by NSAIDs might be benign, or it might blunt the immune system’s ability to fight the disease during the early stages of infection. It could also reduce the magnitude and/or length of protection from either natural infection or vaccination, said Dr. Wilen.
  • The initial motivation to investigate NSAIDs’ effect on C19 “was a twitter thread, suggesting NSAIDs should not be used during C19,” said Dr. Wilen. “This seemed suspicious to us, so we wanted to investigate.”
  • Dr. Wilen and his team expected that there would be little to no effect of NSAIDs on viral infection, which turned out to be correct.They also thought that NSAIDs would not significantly affect the antibody response to natural infection. “In fact, we initially didn’t even carefully look at the antibody response, because we didn’t expect it to be altered by NSAIDs. This turned out to be wrong, said Dr. Wilen.

Source:      https://scitechdaily.com/nsaids-such-as-advil-and-meloxicam-might-exacerbate-or-suppress-covid-19-depending-on-timing/

6.      The immune system mounts a lasting defense after recovery from C19

  • As the number of people who have fought off SARS-CoV-2 climbs ever higher, a critical question has grown in importance: How long will their immunity to the novel coronavirus last? A new Rockefeller study offers an encouraging answer, suggesting that those who recover from C19 are protected against the virus for at least six months, and likely much longer.
  • The findings, published in Nature, provide the strongest evidence yet that the immune system “remembers” the virus and, remarkably, continues to improve the quality of antibodies even after the infection has waned. Antibodies produced months after the infection showed increased ability to block SARS-CoV-2, as well as its mutated versions such as the South African variant.
  • The researchers found that these improved antibodies are produced by immune cells that have kept evolving, apparently due to a continued exposure to the remnants of the virus hidden in the gut tissue.
  • Based on these findings, researchers suspect that when the recovered patient next encounters the virus, the response would be both faster and more effective, preventing re-infection.
  • “This is really exciting news. The type of immune response we see here could potentially provide protection for quite some time, by enabling the body to mount a rapid and effective response to the virus upon re-exposure,” says Michel C. Nussenzweig, the Zanvil A. Cohn and Ralph M. Steinman Professor and head of the Laboratory of Molecular Immunology, whose team has been tracking and characterizing antibody response in C19 patients since the early days of the pandemic in New York.
Long-lasting memory
  • Antibodies, which the body creates in response to infection, linger in the blood plasma for several weeks or months, but their levels significantly drop with time. The immune system has a more efficient way of dealing with pathogens: instead of producing antibodies all the time, it creates memory B cells that recognize the pathogen, and can quickly unleash a new round of antibodies when they encounter it a second time.
  • But how well this memory works depends on the pathogen. To understand the case with SARS-CoV-2, Nussenzweig and his colleagues studied the antibody responses of 87 individuals at two timepoints: one month after infection, and then again six months later. As expected, they found that although antibodies were still detectable by the six-month point, their numbers had markedly decreased. Lab experiments showed that the ability of the participants’ plasma samples to neutralize the virus was reduced by five-fold.
  • In contrast, the patients’ memory B cells, specifically those that produce antibodies against SARS-CoV-2, did not decline in number, and even slightly increased in some cases. “The overall numbers of memory B cells that produced antibodies attacking the Achilles’ heel of the virus, known as the receptor-binding domain, stayed the same,” says Christian Gaebler, a physician and immunologist in Nussenzweig’s lab. “That’s good news because those are the ones that you need if you encounter the virus again.”
Viral stowaways
  • A closer look at the memory B cells revealed something surprising: these cells had gone through numerous rounds of mutation even after the infection resolved, and as a result the antibodies they produced were much more effective than the originals. Subsequent lab experiments showed this new set of antibodies were better able to latch on tightly to the virus and could recognize even mutated versions of it.
  • “We were surprised to see the memory B cells had kept evolving during this time,” Nussenzweig says. “That often happens in chronic infections, like HIV or herpes, where the virus lingers in the body. But we weren’t expecting to see it with SARS-CoV-2, which is thought to leave the body after infection has resolved.”
  • SARS-CoV-2 replicates in certain cells in the lungs, upper throat, and small intestine, and residual viral particles hiding within these tissues could be driving the evolution of memory cells. To look into this hypothesis, the researchers have teamed up with Saurabh Mehandru, a former Rockefeller scientist and currently a physician at Mount Sinai Hospital, who has been examining biopsies of intestinal tissue from people who had recovered from C19 on average three months earlier.
  • In seven of the 14 individuals studied, tests showed the presence of SARS-CoV-2’s genetic material and its proteins in the cells that line the intestines. The researchers don’t know whether these viral left-overs are still infectious or are simply the remains of dead viruses.
  • The team plans to study more people to better understand what role the viral stowaways may play in both the progression of the disease and in immunity.

Source:      https://www.eurekalert.org/pub_releases/2021-01/ru-tis012021.php

E.      Vaccines & Testing

1.      Vaccine Development & Efficacy

  • On January 25, Merck announced that it “is discontinuing development of its SARS-CoV-2/C19 vaccine candidates” as a result of poor performance during Phase 1 clinical trials. While Merck’s 2 candidates were well tolerated from a safety perspective, the immune response generated in the study participants was “inferior to those seen following natural infection and…for other SARS-CoV-2/C19 vaccines.” The Merck vaccines were highly anticipated, as they used viral platforms that could replicate in the human body, which had the potential to confer longer-lasting immunity with a single dose.
  • Despite having already received authorization for the use of its SARS-CoV-2 vaccine in multiple countries, Moderna is already developing a booster to better protect against emerging variants.
  • On January 25, Moderna announced preliminary results from a study assessing the current vaccine’s efficacy against emerging variants, including B.1.1.7 and B.1.351. Compared to reference strains, the vaccine did not exhibit any decrease in neutralizing antibody titers against the B.1.1.7 variant. Conversely, the vaccine exhibited a 6-fold reduction in neutralizing antibodies effective against the B.1.351 variant, which could indicate a lesser degree of protection or faster waning of immunity.
  • A press release from the company indicated that while the immune response was lower, the vaccine did offer some protection. Considering that the immune response from the vaccine appears to be stronger than from natural infection, a moderate decrease in efficacy could still provide a meaningful degree of protection.
  • In response to the concerning results, Moderna announced that it is in the process of developing a new booster that is tailored to provide increased protection against the B.1.351 variant. Additionally, Moderna is testing the effect of a second booster dose of the existing vaccine to determine any additional benefit in terms of protection against the B.1.351 variant. Considering that Moderna’s existing vaccine is already authorized for use in multiple countries, it is unclear what the regulatory review process would look like for a new booster or an additional booster dose.

Source:      Johns Hopkins COVID-19 Update

2.      Vaccines versus the variants

  • Moderna and Pfizer acknowledged today that their vaccines might require alterations and boosters to fend off new and future variants of the virus. It’s a stark admission that the virus is adapting more quickly than previously thought, and that it may continue to mutate in ways that can help it evade vaccines.
  • The British variant had no effect on the levels of neutralizing antibodies — the type that can disable the virus — produced after vaccination. But with the South African form, there was a sixfold reduction in those levels. Even so, Moderna said, those antibodies “remain above levels that are expected to be protective.”
  • Nevertheless, Moderna has already begun developing a new form of the vaccine that could be used as a booster against the South African variant.
  • We’re doing it today to be ahead of the curve, should we need to,” Dr. Tal Zaks, Moderna’s chief medical officer, told The Times. “I think of it as an insurance policy.”
  • Fortunately, the mRNA technology used by Moderna and Pfizer-BioNTech allows the companies to create vaccines much more quickly than traditional methods. The chief executive of BioNTech, Dr. Ugur Sahin, said today that the company could develop a new variant-targeted vaccine in six weeks, though it would be up to regulators to determine the timeline for rolling it out.
  • Scientists have long predicted that the coronavirus would eventually evolve in ways that could thwart vaccines, though few thought it would happen so quickly. Part of the problem is how fast the virus is spreading worldwide, which gives it more opportunities to mutate.
  • Another issue is that few countries — including the U.S. — have invested in the kind of programs that could detect emerging variants, essentially leaving them blind to mutations. The pace of vaccinations, which could eventually provide herd immunity, has also been slow in places like the U.S. and the European Union — and there are many countries in the world where no one has been vaccinated at all.

Source:      New York Times Coronavirus Briefing

F.      Improved & Potential Treatments

1.      Regeneron says antibody cocktail is 100% effective in preventing symptomatic C19 infection 

  • An antibody cocktail used to treat C19 has shown to be 100% effective at protecting against symptomatic cases of the bug, according to new data released Tuesday.
  • Regeneron said its REGEN-COV treatment completely stopped symptomatic infections and cut overall rates of infections to about 50% in about 400 participants who were living with a C19 patient.
  • Ten out of 186 people who received the treatment contracted C19 but did not experience symptoms.
  • Those participants also had smaller viral loads and a shorter period of viral shedding, the company said.
  • The Westchester-based biotechnology giant said the treatment could be used as a “passive vaccine” following the Phase 3 results in the trial jointly run by the National Institute of Allergy and Infectious Diseases.
  • Ten out of 186 people who received the treatment contracted C19 but did not experience symptoms.
  • In November, the FDA green-lit Regeneron’s therapy for mild to moderate C19 cases in adults and children.
  • A “passive vaccine” involves delivering virus-fighting antibodies into the body — unlike traditional vaccines, which activate a person’s immune system to develop their own antibodies.
  • Full results from the trial are expected in the second quarter.

Source:      https://nypost.com/2021/01/26/regeneron-says-passive-covid-19-vaccine-is-100-percent-effective/

2.      Colchicine, a gout drug, shows preliminary promise for C19 

  • A press release from a Canadian research group raised hopes that treating people recently diagnosed with C19 with colchicine, a drug commonly used to treat gout, could reduce the risk they will need to be hospitalized.
  • But outside experts said the data provided were too limited to draw conclusions, leading to discussions of the risks of conducting science via press release, instead of in more detailed manuscripts in peer-reviewed journals. All hoped that colchicine, a cheap and globally available generic medicine with manageable side effects, would prove to be beneficial.
  • In the release, which was issued late Friday, the Montreal Heart Institute said that the rate of hospitalization or death was 21% lower among patients in its COLCORONA study who received colchicine compared to those who were randomly assigned to placebo. The study enrolled 4,488 patients.
  • But here’s a caveat: the press release said these results were not statistically significant, although the numbers are close. When the researchers excluded 329 patients who were diagnosed with C19 based on family contacts or clinical symptoms, but who did not have positive PCR tests, there was a 25% reduction in hospitalization, and substantial reductions in the need for mechanical ventilation and deaths.
  • The press release calls the results “clinically persuasive” and Tardif is quoted in it that colchicine is “the first oral medication in the world whose use could have a significant impact on public health and potentially prevent C19 complications for millions of patients.”
  • There are also other studies testing colchicine, including an arm of the RECOVERY trial, which is evaluating the drug in sicker patients.

Source:    https://www.statnews.com/2021/01/23/colchicine-gout-drug-shows-promise-for-covid-19/

3.      Lilly Antibody Drug Prevents C19 in Nursing Homes 

  • Eli Lilly said its antibody-based drug prevented C19 among many residents and staff of nursing homes and assisted-living facilities, results that point to the drug complementing vaccines while inoculations increase.
  • The drug, called bamlanivimab (“Bam-Bam”), reduced the risk of both staff and residents getting sick with C19 by about 57% compared with a placebo eight weeks after receiving doses, Lilly said Thursday. The effect was more pronounced among residents, the company said, an 80% reduction in risk of C19.
  • Lilly said it would ask U.S. health regulators to widen the drug’s authorized use to include protecting people in long-term-care facilities where someone has recently been diagnosed with C19.
  • In November, the U.S. Food and Drug Administration authorized bamlanivimab to treat people already sick with mild to moderate C19, based on a prior study showing it helped improve symptoms and kept patients out of the hospital.
  • “We want to try to get this to people in nursing homes,” he said in an interview. “It’s not an alternative for a vaccine. It’s for people who haven’t been vaccinated, and there’s an outbreak in their facility—this could be a last resort.”
  • Lilly started the 5,000-subject study in August in U.S. nursing homes that had a recently diagnosed case of C19, putting residents and staff at high risk of exposure. The study is ongoing and is also testing combining bamlanivimab with another antibody.
  • Once a case was diagnosed, other residents and staff were tested for C19 and offered an intravenous infusion of bamlanivimab. For people who tested positive, the study also tracked whether bamlanivimab was effective as a treatment.
  • The prevention data that Lilly released was from 965 people—299 residents and 666 staff—who had tested negative for the virus at the start of the study.
  • Among these residents, four people subsequently contracted the disease and died from it, and all had received a placebo. No residents who tested negative and received the Lilly drug died from the disease, Lilly said.
  • Lilly also is developing additional antibody treatments for C19. The company believes bamlanivimab will still be effective against the coronavirus variant that has spread in the U.K., but has less confidence it can work against a different variant identified in South Africa, Dr. Skovronsky said.
  • Yet he added that Lilly should be able to develop an antibody that would work against the South African variant.

Source:      https://www.wsj.com/articles/lilly-antibody-drug-prevents-covid-19-in-nursing-homes-study-finds-11611234000

4.         New C19 therapy could be ’30 times more potent than Remdesivir’

  • A UCSF-led science team may have found another breakthrough drug treatment to fight C19, as first reported by the San Francisco Chronicle. Studies have shown that small concentrations of Aplidin, a drug created using an extraction from a marine creature called Aplidium albicans, killed the virus in both infected human lung cells and analogous cells from monkeys.
  • The study, which has been published in the journal Science, shows that the “sea squirt” found off the coast of Ibiza could be “almost 30 times more potent than Remdesivir,” the Chronicle reported. While not yet approved to treat patients with C19, if proven effective this treatment would be a welcome addition to the still small amount of antiviral drugs available to treat the disease.
  • The drug, also known as plitidepsin, isn’t commercially available in much of the world, but has already been approved in Australia to treat a type of blood cancer called multiple myeloma. It’s owned by Pharma Mar, a Spanish company founded by a scuba-diving scientist.
  • In a clinical trial in Spain, Pharma Mar reported that 27 patients who were given Aplidin saw a reduced amount of time in the hospital recovering from C19, with 81% of patients returning home within 15 days. The typical rate of return is 47%.
  • Aplidin has also been tested in mice successfully, with the virus effectively disappearing from the body after treatment. Unlike Remdesivir, rather than attacking the virus, the drug could prevent a specific protein inside human cells from replicating the virus.
  • More trials are planned for the U.S. and Spain, Pascal Besman, the company’s chief operating officer, told the Chronicle.

Source:      https://www.sfgate.com/bayarea/article/Aplidin-new-COVID-19-drug-treatment-15896817.php

5.      Nasal spray that blocks C19 could be available by summer 

  • A nasal spray that can prevent C19 for up to two days has been developed by researchers in the UK – and it may be available over the counter by the summer, according to a report.
  • The spray — developed by scientists at the University of Birmingham — prevents infection by capturing the bug in the nose and covering it in a coating from which it cannot escape, The Telegraph reported.
  • As a result, it would be safe for someone to exhale near another person because the virus would be inactive and harmless, the outlet said.
  • Dr. Richard Moakes, the study’s lead researcher, said he was confident that the spray will be able to put an end to social distancing restrictions and “get schools going again.”
  • “We think it will help in schools, as one of the good things about the formulation of the nasal spray is that it would not need to be reformulated for children,” Moakes told The Telegraph.
  • “If it could facilitate getting students back to school, and education being re-established, then that would be great.”
  • The spray includes an antiviral agent called carrageenan — also used as a thickening agent in food — and a solution called gellan, a gelling agent that sticks to cells in the nose.
  • Gellan can be sprayed as fine droplets inside the nasal cavity, where it can cover the surface evenly and stay at the delivery site rather than sliding out of the nose.
  • These ingredients are already approved for medical use, meaning it does not require additional approval, The Telegraph noted.
  • “Based on the product, it will be much quicker to get to the user than a novel drug,” Moakes told the Telegraph.
  • “I am confident that the formulation can make an impact. Our goal is to make an impact as soon as possible. We would really like to see this happen by summer.”
  • The researchers — who have been developing the spray since April 2020 —  are in discussions with shops and pharmaceutical giants on the next steps to mass-produce it, The Telegraph reported. It is unclear when if or when it could become available outside of the UK.
  • The researchers announced in November that lab experiments showed the spray prevented an infection from spreading for up to 48 hours.
  • The scientists believe using it four times a day would be enough for general protection, although it is safe enough to be used every 20 minutes in a high-risk environment such as crowded schools.

Source:      https://nypost.com/2021/01/25/covid-19-blocking-nasal-spray-may-be-available-by-summer/

6.      In preclinical models, antiviral inhibits C19 better than Remdesivir 

·      Working in preclinical models, researchers report that plitidepsin, a drug with limited clinical approval for the treatment of multiple myeloma, is more potent against the coronavirus (SARS-CoV-2) than remdesivir, an antiviral that received FDA emergency use authorization for the treatment of C19 in 2020.

·      The results suggest plitidepsin should be further evaluated as a C19 therapy, the authors say; because it targets a host protein rather than a viral protein, if treatment proves successful in humans, the SARS-CoV-2 virus won’t be easily able to gain resistance against the drug through mutation.

·      The ongoing SARS-CoV-2 pandemic has created the need for antiviral therapeutics that can be swiftly moved into the clinic. This has led researchers to screen clinically approved antivirals. While traditional antivirals, like remdesivir, target viral enzymes that are often subject to mutation, and thus to the development of drug resistance, antivirals that target the cell host proteins required for viral replication could avoid resistance.

·      In earlier work investigating host proteins likely to play a role in the viral life cycle of SARS-CoV-2, including a study in Science in October 2020, Kris White and colleagues found that targeting the host translation machinery that is used in the replication of many viral pathogens could greatly inhibit SARS-CoV-2. Based on this they evaluated plitidepsin, a known inhibitor of a protein involved in host protein translation.

·      In addition to having a limited clinical approval for treating multiple myeloma, it has also successfully completed a phase I/II clinical study for the treatment of C19. Here, in studies in human cells, plitidepsin demonstrated potent anti-SARS-CoV-2 activity – 27.5-fold more so than remdesivir as tested in the same cell line.

·      In a model of human lung cells, plitidepsin greatly reduced viral replication. After further experiments involving remdesivir and plitidepsin in vitro, the researchers suggest that plitidepsin has an additive effect with this approved drug and would be a potential candidate for a combined therapy.

·      The researchers also tested the drug in mice later infected with SARS-CoV-2. Mice who received the drug prophylactically had reduced viral load and lung inflammation compared to control mice. “We believe that our data and the initial positive results from PharmaMar’s clinical trial suggests that plitidepsin should be strongly considered for expanded clinical trials for the treatment of C19,” conclude the authors.

Source:      https://www.eurekalert.org/pub_releases/2021-01/aaft-ipm012521.php

G.      Concerns & Unknowns

1.      Rogue antibodies could be driving severe C19

  • More than a year after C19 emerged, many mysteries persist about the disease: why do some people get so much sicker than others? Why does lung damage sometimes continue to worsen well after the body seems to have cleared the coronavirus (SARS-CoV-2)? And what is behind the extended, multi-organ illness that lasts for months in people with ‘long COVID’? A growing number of studies suggest that some of these questions might be explained by the immune system mistakenly turning against the body — a phenomenon known as autoimmunity.
  • “This is a rapidly evolving area, but all the evidence is converging,” says Aaron Ring, an immunologist at the Yale School of Medicine in New Haven, Connecticut.
  • Early in the pandemic, researchers suggested that some people have an overactive immune response to COVID infection. Immune-system signalling proteins called cytokines can ramp up to dangerous levels, leading to ‘cytokine storms’ and damage to the body’s own cells. Clinical trials have now shown that some drugs that broadly dampen immune activity seem to reduce death rates in critically ill people, if administered at the right time.
  • But scientists studying COVID are increasingly also highlighting the role of autoantibodies: rogue antibodies that attack either elements of the body’s immune defenses or specific proteins in organs such as the heart. In contrast to cytokine storms, which tend to cause systemic, short-duration problems, autoantibodies are thought to result in targeted, longer-term damage, says immunologist Akiko Iwasaki, a colleague of Ring’s at Yale.
  • Even healthy people make autoantibodies, but not generally in large amounts, and the molecules don’t usually seem to cause damage or attack the immune system.
  • Yet researchers also have evidence that nefarious autoantibodies do have a role in many infectious diseases.
  • There are several theories to explain how autoimmunity might emerge from COVID and other infections. Some people might be predisposed to producing autoantibodies that can then wreak havoc during an infection. Alternatively, infections could even trigger the production of autoantibodies. If researchers can establish the link, they might be able to come up with avenues for treatment, both for the repercussions of COVID and for other diseases caused by viruses.
Finding autoantibodies
  • In late September, a group led by Jean-Laurent Casanova at the Rockefeller University in New York City reported that more than 10% of 987 individuals with severe C19 had antibodies that attacked and blocked the action of type 1 interferon molecules, which normally help to bolster the immune response against foreign pathogens. That was a striking proportion, the researchers say, because people’s antibody repertoires are normally very dissimilar, and no one in a control group for the study had these antibodies. The researchers also saw the antibodies in people before their C19 infection, so Casanova thinks that some people could be genetically predisposed to produce them. And the autoantibodies were more common in men than women — a possible factor in why COVID seems to hit men harder.
  • The first evidence suggesting that autoantibodies against interferon might put people at higher risk of infectious disease was published in 1984, and evidence has accumulated since then, Casanova says. But now COVID is drawing more attention to the connection. “Now people understand the problem,” he says, “and all of a sudden they realize that what my lab has been doing for 25 years is actually pretty meaningful.”
  • Casanova is now screening 40,000 people to see how many have pre-existing autoantibodies and determine whether their distribution by age, ancestry and gender matches that of severe COVID.
  • Other research groups have supported Casanova’s autoantibody connection. Iwasaki, Ring and others screened 194 patients and hospital workers with varying severities of COVID for a wide range of autoantibodies. Their study, which was posted online in December and has not yet been peer reviewed, found a higher prevalence of autoantibodies against the immune system in infected individuals than in uninfected people. They found autoantibodies that attacked B cells, as well as some that attacked interferon.
  • But this study also suggested that SARS-CoV-2 might cause the body to generate autoantibodies that attack its own tissues. Some of the infected individuals had autoantibodies against proteins in their blood vessels, heart and brain. This was particularly intriguing because many of the symptoms seen in the pandemic are linked to these organs. It’s unclear whether C19 infection caused the body to start making these autoantibodies or whether infected people had them already. Iwasaki says they are hoping to study other cases to establish whether there is a causal link; that would require obtaining more blood samples from before people become infected.
  • Researchers have also found autoantibodies against molecules called phospholipids, adds Michel Goldman, an immunologist at the Free University of Brussels and former director of Europe’s Innovative Medicines Initiative. The largest such study, published in November, found that 52% of 172 people hospitalized with C19 had these autoantibodies. “That’s a real concern,” he says, because some phospholipids are known to have a role in controlling blood clotting, which goes awry in C19.
  • This month, another study, not yet peer reviewed, reported finding autoantibodies that might be spurred by C19. David Lee, an emergency-medicine doctor at New York University (NYU) Langone Health, partnered with NYU microbiologist Ana Rodriguez and others to analyse serum samples from 86 people hospitalized with C19. They looked for autoantibodies against proteins such as annexin A2, which is of particular interest because it helps to keep cell membranes stable and ensures the integrity of small blood vessels in the lungs. The researchers found a significantly higher average level of anti-annexin A2 antibodies in people who had died than in those with non-critical illness. As with other studies, it’s still unclear whether these autoantibodies existed before infection with the coronavirus.
  • The autoantibody theory might explain some of the delay in the onset of severe symptoms in C19. If evoked by the cellular damage and inflammation stoked by viral infection, as Lee and others think, autoantibodies would take a couple of weeks to build up in the body. This, he says, could be why much of the damage to tissues such as the lungs appears so long after a person develops symptoms such as fever. In this way, autoimmunity might be the real culprit behind the deadly destruction that continues after the coronavirus has cleared. “Clinicians are thinking, ‘Oh, this virus is so deadly, we’ve got to get rid of the virus.’ But then when you talk to the pathologists, they’re like, ‘Yeah, so we’re seeing all this damage, but not seeing much virus,’” Lee says.
An infectious idea
  • Over the years, scientists have identified numerous instances of infections generating autoimmunity. Some reports suggest that infection with the malaria parasite can cause the body to begin attacking red blood cells, causing anaemia. And Epstein–Barr virus — which causes glandular fever (also known as mononucleosis) — has been implicated in dozens of autoimmune illnesses, including lupus. Finding a rock-solid connection can be tough, because it’s difficult to show whether the infections are the cause of autoimmune disorders or whether they crop up in the body for another reason, says Anish Suri, president of Cue Biopharma, a company in Cambridge, Massachusetts, that is researching therapies to counter autoimmunity.
  • Strep throat is a well-established example. If left untreated, this illness, which is caused by the bacterium Streptococcus pyogenes, can prompt an autoimmune reaction, known as rheumatic fever, that attacks organs and can lead to permanent heart damage. Other bacteria are also likely to lead to autoimmunity: the stomach bug Helicobacter pylori is thought to cause a disorder called immune thrombocytopenic purpura (ITP), in which the body starts destroying platelets in the blood. In some people with ITP, treatment with antibiotics against H. pylori improves platelet count, suggesting that the drugs help to reverse the autoimmune condition.
  • Another theory is that inflammation caused by an infection might prime the immune system to mistakenly see the spewed contents of destroyed cells as ‘foreign’ and create autoantibodies against these cellular pieces, says Leona Gilbert, a molecular biologist who is a consultant at a diagnostic company named Te?ted Oy in Finland, which has developed and sells a test for SARS-CoV-2 antibodies. The tissue damage that accompanies inflammation is a recipe for the body to begin attacking itself, Gilbert says: “That just precipitates the whole event in developing autoimmune conditions,” she says.
  • Lee, the researcher who studied annexin A2, says the evidence that infections can give rise to autoimmunity is not receiving enough attention. “It should make us rethink dozens of diseases, if not hundreds,” he says. “I’m like, ‘How is anybody not seeing this?’”
Rethinking treatments
  • If an autoimmunity element exists either in predisposing people to C19 or in the fallout from the infection, there might be treatment implications. Casanova says that in cases in which pre-existing autoimmunity against interferon might put people at greater risk of falling ill, then blood tests for autoantibodies, which are becoming more available in research laboratories and university hospitals, could help to identify them.
  • And if these people become infected with SARS-CoV-2, Casanova suggests, they could receive supplementation as early as is practical with interferon-β, which is not as prone to attack from the immune system as are other interferons. Last November, a preliminary study found that an inhaled form of interferon-β seemed to improve the clinical condition of people with COVID, prompting a larger trial of this therapy.
  • Interferon replacements are intended to boost the activity of a weakened immune system. But if autoantibodies attack organs such as the lungs and brain, a blunt strategy for combating them might be to suppress the immune system.
  • Even before autoantibodies came into focus, the idea that a cytokine storm might be a culprit meant that studies were under way to see whether immunosuppressive steroids such as dexamethasone, or the arthritis drugs tocilizumab and sarilumab, could be used to calm immune systems set awry by COVID. The World Health Organization now “strongly recommends” the use of dexamethasone in severe cases, and the United Kingdom is using the arthritis drugs for people with severe COVID after a clinical trial on 7 January10 suggested that they cut death rates in patients in intensive care.
  • Physicians emphasize that, whether they are used to quell a cytokine storm or to try to address autoimmunity, administration of the drugs needs to be carefully timed so that they don’t interfere with the body’s battle against SARS-CoV-2. Suri notes that broad-spectrum immunosuppressants make the body more prone to infection. His company is one of a handful conducting preclinical work to develop engineered molecules that go after specific immunity pathways, rather than suppress immunity across the board.
  • Lee, meanwhile, says that if autoantibodies against annexin A2 and other proteins prove to be a consequence of C19, then it might make sense to study what happens when patients’ plasma is run through a process that clears these antibodies out before returning the plasma.
  • Scientists are very interested in understanding whether autoimmunity is linked to long COVID, too. “First of all, we don’t know if these autoantibodies contribute to long COVID, but if they do, what is the longevity? How long will they last? How long is the body going to keep producing those antibodies?” Ring says. But answering these questions is a complicated endeavour, because people naturally produce many different kinds of antibody, including autoantibodies.
  • Ring hopes that research into viruses and autoimmunity will eventually get much-needed answers for individuals with post-viral autoimmunity, which might include those with C19. “These patients are just so frustrated,” he says. “Their physicians don’t believe them and so they get psych referrals. Just to be able to tell these people they have a real disease and here’s what’s causing it — that would be really meaningful.”

Source:      https://www.nature.com/articles/d41586-021-00149-1

2.      Patients in cancer remission at high risk for severe C19 illness 

  • Patients with inactive cancer and not currently undergoing treatments also face a significantly higher risk of severe illness from C19, a new study from Penn Medicine published online today in JNCI Cancer Spectrum shows. Past reports have established an increased risk of severe disease and death for sick or hospitalized cancer patients with C19 compared to patients without cancer, but less is known about patients in the general population.
  • The findings underscore the importance of C19 mitigation, like social distancing and mask wearing, and vaccinations for all patients, not just those recently diagnosed or with active disease.
  • “Patients who have cancer need to be careful not to become exposed during this time,” said senior author Kara N. Maxwell, MD, PhD, an assistant professor of Hematology-Oncology and Genetics in the Perelman School of Medicine at the University of Pennsylvania and a member of the Abramson Cancer Center and the Basser Center for BRCA. “That message has been out there, but these latest findings show us it’s not only for patients hospitalized or on treatment for their cancer. All oncology patients need to take significant precautions during the pandemic to protect themselves.”
  • The researchers analyzed the records of more than 4,800 patients who had been tested for C19 from the Penn Medicine BioBank, a centralized bank of samples and linked data from the health system’s electronic health records, to investigate the association between cancer status and C19 outcomes. Of the 328 positive cases through June 2020, 67 (20.7 percent) had a cancer diagnosis in their medical history (80.6 percent with solid tumor malignancy and 73.1 percent with inactive cancer).
  • Notably, the proportion of Black patients — who make up 20 percent of the patients in the biobank — was significantly higher in both cancer and non-cancer C19-positive patients (65.7 percent and 64.1 percent, respectively) compared to all patients tested for SARS-CoV-2.
  • The findings parallel prior reports showing the disproportionate impact of C19 on minority communities.
  • “We really need to be thinking about race as a significant factor in trying to get people vaccinated as soon as we can,” Maxwell said.
  • Studies show that cancer patients have a higher risk of C19 complications, due in part to factors such as older age, higher smoking rates, comorbidities, frequent health care exposures, and the effects of cancer therapies. These latest results also suggest the cancer itself and its impact on the body may play a role in exacerbating C19 infections.
  • “Our finding that cancer patients with C19 were more likely than non-cancer patients to experience hospitalization and death even after adjusting for patient-level factors supports the hypothesis that cancer is an independent risk factor for poor C19 outcomes,” they wrote.
  • In a separate, related study published in the preprint database bioRxiv and not yet peer-reviewed, Penn Medicine researchers report that cancer patients receiving in-person care at a facility with aggressive mitigation efforts have an extremely low likelihood of C19 infection. Of 124 patients in the study receiving treatment at Penn Medicine, none tested positive for the virus after their clinical visits (an average of 13 per patient).
  • The results suggest those efforts, when combined with social distancing outside the healthcare setting, may help protect vulnerable cancer patients from C19 exposure and infection, even when ongoing immunomodulatory cancer treatments and frequent healthcare exposure are necessary, the authors said.

Source:      https://www.eurekalert.org/pub_releases/2021-01/uops-pic011821.php

3.      Covid linked to risk of mental illness and brain disorder 

One in eight people who get coronavirus also have first psychiatric or neurological illness within six months, research finds
  • The analysis – which is still to be peer-reviewed – also found that those figures rose to one in three when patients with a previous history of psychiatric or neurological illnesses were included.
  • It found that one in nine patients were also diagnosed with things such as depression or stroke despite not having gone to hospital when they had C19, which was surprising, said the lead author, Dr Max Taquet of the department of psychiatry at the University of Oxford.
  • The researchers used electronic health records to evaluate 236,379 hospitalised and non-hospitalised US patients with a confirmed diagnosis of C19 who survived the disease, comparing them with a group diagnosed with influenza, and a cohort diagnosed with respiratory tract infections between 20 January and 13 December 2020.
  • The analysis, which accounted for known risk factors such as age, sex, race, underlying physical and mental conditions and socio-economic deprivation, found that the incidence of neurological or psychiatric conditions post-Covid within six months was 33.6%. Nearly 13% received their first such diagnosis.
  • The data adds to prior research by Taquet and others that showed nearly one in five people who have had C19 are diagnosed with a psychiatric disorder within three months of testing positive for the virus.
  • Overall, C19 was associated with increased risk of these diagnoses, but the incidence was greater in patients who required hospital treatment, and markedly so in those who developed brain disease.
  • Although the study does not prove that C19 is directly behind these psychiatric and neurological conditions, research that suggests the virus can have an impact on the brain and the central nervous system is emerging.
  • The analysis should also be also interpreted with caution, given it is possible that the first entry of a diagnosis into the electronic database might not represent the first occurrence of the condition. Such records are also typically lacking in other relevant information such as housing density, family size, employment and immigration status.
  • Dr Tim Nicholson, a psychiatrist and clinical lecturer at King’s College hospital who was not involved in the analysis, said the findings would help steer researchers in the direction of which neurological and psychiatric complications required further careful study.
  • “I think particularly this raises a few disorders up the list of interests, particularly dementia and psychosis … and pushes a few a bit further down the list of potential importance, including Guillain-Barré syndrome.”

Source:      https://www.theguardian.com/world/2021/jan/25/covid-linked-to-risk-of-mental-illness-and-brain-disorder-study-suggests

4.      Examining Infection Fatality Rates: C19 Is Dangerous for Middle-Aged Adults, Not Just the Elderly 

  • C19 has been spreading rapidly over the past several months, and the U.S. death toll has now reached 400,000. As evident from the age distribution of those fatalities, C19 is dangerous not only for the elderly but for middle-aged adults, according to a Dartmouth-led study published in the European Journal of Epidemiology.
  • “For a person who is middle-aged, the risk of dying from C19 is about 100 times greater than dying from an automobile accident,” explains lead author Andrew Levin, a professor of economics at Dartmouth College. “Generally speaking, very few children and young adults die of C19. However, the risk is progressively greater for middle-aged and older adults. The odds that an infection becomes fatal is only 1:10,000 at age 25, whereas those odds are roughly 1:100 at age 60, 1:40 at age 70, and 1:10 at age 80.”
  • These findings represent the culmination of a systematic review of all available studies of C19 prevalence in countries with advanced economies; this review encompassed more than 1,000 research papers and government documents disseminated prior to September 18, 2020. The research team identified 27 studies where the survey design was representative of the general population, covering 34 geographical locations in the U.S., Canada, Asia, and Europe. Using those prevalence data, the researchers investigated the age-specific ratio of C19 fatalities to infections and found a very clear exponential relationship.
  • An initial version of this study was posted online in July 2020 as an NBER Working Paper and was regularly updated on the medRxiv preprint server prior to being published as an open-access article in the European Journal of Epidemiology. The findings remain highly relevant as the total number of C19 deaths in the U.S. continues to climb. “Our findings are consistent with the CDC’s Weekly Updates by Select Demographic and Geographic Characteristics, which report on C19 deaths by age group,” says Levin. “Nearly 40 percent of U.S. C19 deaths have occurred among those ages 45 to 74 years, while almost 60 percent have occurred among those over 75 years old. By contrast, children and young adults (less than 45 years old) account for less than 3 percent of U.S. C19 deaths.”
  • Levin also emphasized the urgent practical implications of his team’s research findings. “While C19 vaccines are now being distributed, several more months are likely to pass before these vaccines have been fully disseminated to the public,” says Levin. “We need get through this period as safely as possible. Taking basic precautions–including wearing a mask, practicing social distancing, and washing your hands often–is critical to protecting yourself, family, friends, and community members from this very deadly disease.”

Source:      https://scitechdaily.com/examining-infection-fatality-rates-covid-19-is-dangerous-for-middle-aged-adults-not-just-the-elderly/

5.      C19 virus helps block host immunity 

  • The coronavirus (SARS-CoV-2) blocks the processes of innate immune activation that normally direct the production and/or signaling of type I interferon (IFN-I) by the infected cell and tissues. IFN-I is a key component of host innate immunity that is responsible for eliminating the virus at the early stage of infection, as summarized in a recent review article in Journal of Interferon & Cytokine Research (JICR). By suppressing innate immunity, the virus replicates and spreads in the body unchecked, leading to C19. Click here to read the article now.
  • “SARS-CoV-2 utilizes various approaches to evade host IFN-I response, including suppression of IFN-I production and IFN-I signaling,” state Hongjie Xia and Pei-Yong Shi, University of Texas Medical Branch at Galveston. “Viruses defective in antagonizing IFN-I response, in combination with replication-defective mutations, could potentially be developed as live attenuated vaccine candidates.”
  • “Targeting innate immunity is highly attractive for therapeutic and vaccine strategies aimed at controlling SARS-CoV-2 infection and protecting against C19. By revealing how the virus blocks innate immune programs we can then build approaches to restore these processes and enhance antiviral immunity,” says Journal of Interferon & Cytokine Research Editor-in-Chief Michael Gale Jr., Department of Immunology and Center for Innate Immunity and Immune Disease, University of Washington.
  • Ricardo Pereda and coauthors explore the therapeutic effectiveness of interferon alpha 2b treatment for C19 patient recovery. They showed that interferon treatment decreases the likelihood of intensive care stay and increases patient survival after severe or critical disease.

Source:      https://www.eurekalert.org/pub_releases/2021-01/mali-cvh012121.php

6.      Lifetime smoking history associated with C19 severity

  • How much someone has ever smoked — even if they’ve quit — has a significant bearing on their risk of becoming hospitalized or dying after C19 infection.
  • A new study that measured smoking in pack years among more than 7,100 C19 patients diagnosed from March through August 2020 found that people who smoked the most were more than twice as likely to need hospitalization and almost twice as likely to die compared with never smokers.
  • Adjusting for other conditions the smokers had lowered the odds somewhat, but the authors maintain that cumulative exposure to cigarette smoke is an independent risk factor for hospital admission and death from C19.

Source:      Stat News

H.      Back to School!?

1.         CDC officials say most available evidence indicates schools can be safe if precautions are taken on campus and in the community

  • When to keep schools open, and how to do so, has been an issue plaguing the response by the United States to the pandemic since its beginning. President Biden vowed to “teach our children in safe schools” in his inaugural address.
  • On Tuesday, federal health officials weighed in with a call for returning children to the nation’s classrooms as soon as possible, saying the “preponderance of available evidence” indicates that in-person instruction can be carried out safely as long as mask-wearing and social distancing are maintained.
  • But local officials also must be willing to impose limits on other settings — like indoor dining, bars or poorly ventilated gyms — in order to keep infection rates low in the community at large, researchers at the Centers for Disease Control and Prevention said in the journal JAMA and in a follow-up interview.
  • School administrators must limit risky activities such as indoor sports, they added. “It’s not going to be safe to have a pizza party with a group of students,” Margaret Honein, a member of the C.D.C.’s C19 emergency response team and the first author of the article, said in an interview. “But outdoor cross-country, where distance can be maintained, might be fine to continue.”
  • Federal officials cited the many benefits of in-person schooling for children, and argued for prioritizing their educational, developmental and emotional and mental health needs. “Schools are an important source not just of education, but health and social services for children,” Dr. Honein said.
  • Even though the pandemic is rapidly changing, and contagious new variants are spreading, Dr. Honein and other C.D.C. officials argued there is little evidence that schools spark the kind of outbreaks seen in nursing homes and meatpacking plants, or contribute to increased transmission in communities.
  • “Back in August and September, we did not have a lot of data on whether or not we would see the same sort of rapid spread in schools that we had seen in other high-density work sites or residential sites,” Dr. Honein said. “But there is accumulating data now that with high face mask compliance, and distancing and cohorting of students to minimize the total number of contacts, we can minimize the amount of transmission in schools.”
  • The call by Dr. Honein and other officials reflects a consensus among some leading educators and public health experts that schools should be the last to close and the first to open when shutdowns are necessary.
  • Last year, all kindergarten to grade 12 public schools closed for in-person instruction by March 25, shortly after the World Health Organization declared that the new coronavirus outbreak was a pandemic. Many schools subsequently switched to online teaching models for the rest of the school year.
  • During the fall term, about one-quarter of school districts were completely online, about half were using a hybrid model, and fewer than one-quarter were fully open for in-person teaching. Yet more than half of school districts had students participating in sports programs.
  • In an opinion column in USA Today earlier this week, Randi Weingarten, the president of the American Federation of Teachers, and Dr. Rajiv Shah, president of the Rockefeller Foundation, called for widespread testing to keep schools safe and get children back into the classroom, not only for educational reasons, but to restore free school meals, give children a social outlet, and provide myriad school-based services that are vital to low-income children.
  • The C19 School Response Dashboard, a collaboration that tracks infections in school districts willing to share data, has reported that infection case rates among staff in October and November were similar to case rates in the surrounding communities. More recently, however, staff case rates in New York increased at a faster rate than community case rates.
  • The causes are not clear. The increases may reflect a more frequent testing of schoolteachers. Case rates increased among teachers engaged in in-person teaching and among those teaching remotely, suggesting in-person instruction was not the sole factor.
  • Emily Oster, a professor of economics and public policy at Brown University who created the dashboard, said that low case rates in the community make it possible to keep schools running safely.
  • “Prioritizing schools is going to mean limiting some of those other activities, and deciding that we want to undertake some of those sacrifices to keep schools open, because we’ve decided as a society that schools are important relative to other things,” Dr. Oster said.
  • “The frustration for many people is that you can go to an indoor restaurant. In Massachusetts, I could go to an indoor water park like Great Wolf Lodge — I can take my kids to Great Wolf Lodge. But in a lot of places in Massachusetts, there has been no school.”
  • The C.D.C. also published two related studies on Tuesday. One was an investigation of a high school wrestling tournament in Florida in December that became a super-spreader event, leading to at least 79 infections and one death.
  • The tournament brought together 10 schools and 130 athletes and coaches, and 30 percent of participants were infected with the coronavirus. Thirty-eight individuals went on to transmit the virus to at least 41 others, including family members. (The full number is not yet known, because fewer than half the participants were tested.)
  • The researchers calculated that 1,700 in-person school days were lost to quarantines and isolation of patients and their contacts. The number would have been higher if not for the December holiday break.
  • C.D.C. researchers also took a look at 17 elementary and secondary schools in rural Wisconsin where mask-wearing was routine. The incidence of infection was lower in schools than in the community at large, the scientists found. During 13 weeks in the fall of 2020, there were 191 infections among staff and students; only seven resulted from in-school transmission, according to the study.

Source:      New York Times Coronavirus Update

2.         What new COVID variants mean for schools is not yet clear

  • ●      The emergence of fast-spreading coronavirus variants has once again put a spotlight on the role of children in the C19 pandemic. Early data on one new variant had suggested that it was spreading more in children than in adults compared with other lineages. But researchers now suggest the variant is spreading more efficiently in all age groups, allaying those fears.
  • Still, a year into the pandemic, much remains unknown about the spread of the coronavirus (SARS-CoV-2) in children, prompting calls for increased surveillance and testing to inform decisions about school closures. “We still don’t really know how much schools and children actually contribute to spread,” says Catherine Bennett, an epidemiologist at Deakin University in Melbourne.
  • Children seem to be less susceptible to SARS-CoV-2 than adults are, possibly because of inherent biological differences, says Calum Semple, an outbreak specialist at the University of Liverpool, UK. And studies in schools in several countries last year suggested that campuses were not hot spots for transmission, provided they took precautions such as maintaining hygiene and social distancing. However, data often aren’t easily comparable between countries because of the variation in practices.
  • But if the new variant is increasing infection rates in children, then the dynamics of transmission in schools should be reinvestigated, says Bennett. Better data are needed because cases in children — who more often experience asymptomatic infections — are probably being missed. Countries often test only people with symptoms.
  • Many researchers caution against closing schools before other parts of society, noting the harm to children from missed learning. Other scientists think that governments should act quickly when there is a rise in infections, including closing schools. George Milne, who leads C19 modelling at the University of Western Australia in Perth says: “It’s better to go hard early and [then] relax.”
A changing picture
  • Data collected between late November and mid-December suggested that children were being infected with B.1.1.7, compared with other known lineages, more-so than people in other age groups. This prompted suggestions the variant was spreading in children more easily than in adults.
  • But a January report from Public Health England, a government public-health agency, found that the variant, which has spread to dozens of countries, transmits more easily in all age groups. It also found that children — especially those under the age of ten — are about half as likely as adults to transmit the variant to others.
  • A similar picture is emerging about another fast-spreading variant, which was first detected in South Africa and is known as 501Y.V2, says Richard Lessells, an infectious-diseases specialist at the University of KwaZulu-Natal in Durban. “There’s nothing jumping out at us that there’s different outcomes in the younger group[s],” he says.

Source:      https://www.nature.com/articles/d41586-021-00139-3

I.       Innovation & Technology

1.      Researchers are developing color-changing stickers to detect C19

  • UCSD developing mask-borne sensor that detects the coronavirus. The test strip will help determine if the wearer has the disease or has been exposed to it.
  • The National Institutes of Health has awarded UC San Diego $1.3 million to develop a small, wearable sensor that can tell whether a person has the novel coronavirus or has been exposed to it by someone else.
  • The lightweight sensor would be attached to facemasks to monitor for the presence of coronavirus-related molecules that appear in a person’s breath and saliva.
  • The “surveillance” test strip also would detect virus molecules expelled by someone else and possibly inhaled by the user of the mask.
  • The user would squeeze the sensor to see if it turns color, denoting a positive reading. The process is similar to the one used to check results in a home pregnancy test.
  • If there’s a positive reading, the facemask user would then get a test to confirm the infection. The result would be available almost immediately. The sensor also is meant to be useful in contact tracing.

Source:      https://www.sandiegouniontribune.com/news/science/story/2021-01-21/nih-uc-san-diego-mask-sensors-coronavirus

J.       Projections & Our (Possible) Future

1.      New C19 Model Shows Little Benefit in Vaccinating High-Risk Individuals First 

  • Health authorities face a tenuous balancing act: how to enact policies to keep citizens safe while doing the least possible damage to quality of life and local economies, especially in smaller cities and towns, where short supply of intensive care units and tight budgets make the thin line between precautionary measures and normalcy even thinner.
  • A new theory and simulation platform that can create predictive models based on aggregated data from observations taken across multiple strata of society could prove invaluable. 
  • Developed by a research team led by Maurizio Porfiri, Institute Professor at the NYU Tandon School of Engineering, the novel open-source platform comprises an agent-based model (ABM) of C19 for the entire town of New Rochelle, located in Westchester County in New York State.
  • The ABM replicates, geographically and demographically, the town structure obtained from U.S. Census statistics and superimposes a high-resolution — both temporal and spatial — representation of the epidemic at the individual level, considering physical locations as well as unique features of communities, like human behavioral trends or local mobility patterns.
  • Among the study’s findings are those suggesting that prioritizing vaccination of high-risk individuals has only a marginal effect on the number of C19 deaths. To obtain significant improvements, a very large fraction of the town population should, in fact, be vaccinated.
  • Importantly, the benefits of the restrictive measures in place during the first wave greatly surpass those from any of these selective vaccination scenarios. Even with a vaccine available, social distancing, masks, and mobility restrictions will still be key tools to fight C19.
  • Porfiri pointed out that focusing on a city of New Rochelle’s size was crucial to the research because most cities in the U.S. have comparable population sizes and concentrations.
  • “We chose New Rochelle not only because of its place in the COVID timeline, but because agent-based modelling for mid-size towns is relatively unexplored despite the U.S. being largely composed of such towns and small cities,” he said.
  • Supported by expert knowledge and informed by officially reported C19 data, the model incorporates detailed elements of pandemic spread within a statistically realistic population. Along with testing, treatment, and vaccination options, the model also accounts for the burden of other illnesses with symptoms similar to those of C19.
  • Unique to the model is the possibility to explore different testing approaches — in hospitals or drive-through facilities— and vaccination strategies that could prioritize vulnerable groups.
  • “We think decision making by public authorities could benefit from this model, not only because it is ‘open source,’ but because it offers a ‘fine-grain’ resolution at the level of the individual and a wide range of features,” noted Porfiri.

Source:    https://scitechdaily.com/hold-up-new-covid-19-model-shows-little-benefit-in-vaccinating-high-risk-individuals-first/

But see:     Why older adults must go to the front of the vaccine line

2.      C19 model reveals key role for innate immunity in controlling viral load 

  • Researchers reporting in ACS Pharmacology & Translational Science have developed a mathematical model of C19 that reveals a key role for the innate immune system in controlling viral load.
  • The C19 pandemic has created tremendous socioeconomic problems and caused the death of almost 2 million people worldwide. Although vaccines are now being administered, few effective therapeutics currently exist. To identify new therapies, scientists need to gain a better understanding of how the virus interacts with the host’s immune system.
  • There are two main branches of the immune system: innate (in which immune cells engulf pathogens, release chemical signals or otherwise respond non-specifically to a pathogen) and adaptive (in which lymphocytes produce antibodies and kill specific pathogens). It’s difficult to study virus dynamics in the human body, so some researchers have developed mathematical models to investigate virus-host interactions. Prashant Dogra, Zhihui Wang and colleagues wanted to improve upon the existing models to simulate the whole-body dynamics of SARS-CoV-2 infection.
  • The researchers developed a mathematical model that predicts the viral load over time in organs that express the ACE-2 receptor, which is necessary for SARS-CoV-2’s entry into cells. Some of the parameters used in the model, such as the levels of various immune cells in the human body, were already known, whereas others, such as the infection rate of target cells, were estimated from published experimental data from C19-infected hamsters.
  • Once the team had developed a simplified model, they used human data to make a more complete one that also included adaptive immunity. When the researchers used the model to simulate different conditions, they found that innate immunity played a larger role in controlling viral load than adaptive immunity, and that it was important to begin antiviral or interferon therapy as soon as possible after the onset of symptoms.
  • The authors acknowledge funding from the National Science Foundation and the National Institutes of Health.
  • The abstract that accompanies this paper is available here.

Source:      https://www.eurekalert.org/pub_releases/2021-01/acs-cmr012021.php

K.      Lockdowns

1.      Another Study Shows—Yet Again—That Lockdowns Don’t Work 

Although advocates for C19 lockdowns continue to insist that they save lives, actual experience keeps suggesting otherwise.
  • On a national level, just eyeballing the data makes this clear. Countries that have implemented harsh lockdowns shouldn’t expect to have comparatively lower numbers of C19 deaths per million.
  • In Italy and the United Kingdom, for example, where lockdowns have been repeatedly imposed, death totals per million remain among the worst in the world. Meanwhile, in the United States, states with the most harsh lockdown rules—such as New York, New Jersey, and Massachusetts are among the states with the worst total deaths.
  • Lockdown advocates, of course, are likely to argue that if researchers control for a variety of other variables, then we’re sure to see that lockdowns have saved millions of lives. Yet research keeps showing us this simply isn’t the case.
  • The latest study to show the weakness of the pro-lockdown position appeared this month in the European Journal of Clinical Investigation, authored by Eran Bendavid, Christopher Oh, Jay Bhattacharya, and John P.A. Ioannidis. Titled “Assessing Mandatory Stay-at-Home and Business Closure Effects on the Spread of C19,” the authors compare “more restrictive non-pharmaceutical interventions” (mrNPI) and “less restrictive non-pharmaceutical interventions” (lrNPI). More restrictive interventions include mandatory stay-at-home orders and forced business closures. Less restrictive measures include “social distancing guidelines, discouraging of international and domestic travel, and a ban on large gatherings.” The researchers compare outcomes at the subnational level in a number of countries, including England, France, Germany, Iran, Italy, the Netherlands, Spain, and the United States. This is then compared against countries with less restrictive measures, primarily Sweden and South Korea, where stay-at-home orders and business closures were not widely implemented.
  • The conclusion:
    • We find no clear, significant beneficial effect of mrNPIs on case growth in any country….In none of the 8 countries and in none out of the 16 comparisons (against Sweden or South Korea) were the effects of mrNPIs significantly negative (beneficial). The point estimates were positive (point in the direction of mrNPIs resulting in increased daily growth in cases).
  • That is, the more restrictive lockdown measures pointed to worse outcomes.
  • This data suggests that the theoretical underpinnings of the lockdown philosophy are wrong. As summed up by Bendavid et al.,
    • The conceptual model underlying this approach is that, prior to meaningful population immunity, individual behavior is the primary driver of reductions in transmission rate, and that any NPI may provide a nudge towards individual behavior change, with response rates that vary between individuals and over time. lrNPIs could have large anti-contagion effects if individual behavioral response is large, in which case additional, more restrictive NPIs may not provide much additional benefit. On the other hand, if lrNPIs provide relatively small nudges to individual behavior, then mrNPIs may result in large behavioral effects at the margin, and large reductions in the growth of new cases.
  • Translation: mild measures encouraging caution on exposure to others probably lessen the spread. Therefore, more stringent measures will surely do an even better job of limiting the spread!
  • But this doesn’t appear to be the case. Rather, the authors suggest those areas with lower covid mortality are areas where the public pursued low-hanging fruit in terms of slowing the spread. This included canceling large, crowded events and limiting travel. More stringent requirements on top of this appeared to produce no beneficial effect, and, if anything, had the opposite of the intended effect.
  • This study, of course, is just the latest in a long line of similar studies calling into question the assumption—for it is only an assumption—that harsh lockdowns lower mortality.
  • For example, back in May, researchers at The Lancet concluded that “hard lockdowns” don’t “protect old and frail” people, nor do they decrease mortality from C19. Later, a July study in The Lancet stated: “The authors identified a negative association between the number of days to any lockdown and the total reported cases per million, where a longer time prior to implementation of any lockdown was associated with a lower number of detected cases per million.”
  • In an August 1 study, also published by The Lancet, the authors concluded, “Rapid border closures, full lockdowns, and wide-spread testing were not associated with C19 mortality per million people.”
  • A June study published in Advance by Stefan Homburg and Christof Kuhbandner found that the data “strongly suggests” that
    • the UK lockdown was both superfluous (it did not prevent an otherwise explosive behavior of the spread of the coronavirus) and ineffective (it did not slow down the death growth rate visibly).
  • In fact, the overall trend of infection and death appears to be remarkably similar across many jurisdictions regardless of what nonpharmaceutical interventions (NPIs) are implemented by policymakers.
  • In a paper published with the National Bureau of Economic Research (NBER), authors Andrew Atkeson, Karen Kopecky, and Tao Zha found that C19 deaths followed a similar pattern “virtually everywhere in the world” and that “[f]ailing to account for this familiar pattern risks overstating the importance of policy mandated NPIs for shaping the progression of this deadly pandemic.”
  • Refusing to be daunted by these holes in the official narrative, lockdown advocates often insist that lockdowns must be tolerated because “it’s better to be safe than sorry.”
  • But this is a highly questionable notion as well.
  • Lockdowns and other forms of mandated isolation bring with them a host of health problems of their own. As Bendavid et al. note, restrictive NPIs:
    • Includ[e] hunger, opioid-related overdoses, missed vaccinations, increase in non-COVID diseases from missed health services, domestic abuse, mental health and suicidality, as well as a host of economic consequences with health implications—it is increasingly recognized that their postulated benefits deserve careful study.
  • Perhaps not surprisingly, data on excess mortality during the C19 pandemic suggests only two-thirds of excess mortality can be medically connected to C19. As explained in a study in JAMA:
    • “Some people who never had the virus may have died because of disruptions caused by the pandemic,” says Dr. Steven H. Woolf, the director emeritus of the Virginia university’s Center on Society and Health and first author of the study. “These include people with acute emergencies, chronic diseases like diabetes that were not properly cared for, or emotional crises that led to overdoses or suicides.”
  • Increases in dementia deaths were especially notable.
  • And these effects can also be felt in the long term. As I showed in an April 30 article, unemployment kills. Economic crises, such as this one that was made worse by mandatory shutdowns and stay-at-home orders, leads to countless “years of life lost” through more suicide, heart disease, and drug overdoses.
  • Moreover, given the nature of the shutdowns and who is affected, this has lopsidedly affected women and especially Hispanic women, who are heavily represented in the workforce behind the service industry businesses shut down by government-imposed business closures.
  • The cumulative effect can be quite large. In a new study from Francesco Bianchi, Giada Bianchi, and Dongho Song from the National Bureau of Economic Research, the authors conclude that the economic fallout—in terms of unemployment and its effects—will lead to nearly nine hundred thousand deaths over the next fifteen years.
  • Of course, not all of the economic pain that coincided with the C19 panic of 2020 can be blamed on forced shutdowns. Many people would have likely minimized contact with others voluntarily out of fear of the disease. This would have indeed caused economic distortions and greater unemployment in some sectors.
  • But, as Bianchi, Bianchi, and Song admit, the lockdowns “contributed to further reduce economic activity” above and beyond normal voluntary reactions to C19. Combining these facts with what we know from the new Bendavid et al. study—namely that voluntary measures accomplished the bulk of mitigation—suggests the “further reduction” in economic activity produced no additional health benefits. That is, the portion of economic destruction wrought by forced shutdowns was inflicted upon the public for nothing.
  • Prior to 2020, of course, this was common knowledge. In a 2006 paper in Biosecurity and Bioterrorism called “Disease Mitigation Measures in the Control of Pandemic Influenza” by Thomas V. Inglesby, Jennifer B. Nuzzo, Tara O’Toole, and D.A. Henderson, the authors conclude:
    • The negative consequences of large-scale quarantine are so extreme (forced confinement of sick people with the well; complete restriction of movement of large populations; difficulty in getting critical supplies, medicines, and food to people inside the quarantine zone) that this mitigation measure should be eliminated from serious consideration.
  • Yet, “public health” bureaucrats suddenly decided in 2020 that decades of research was to be thrown out the window and lockdowns were to be imposed on hundreds of millions of human beings.
Mandatory Lockdowns vs. Voluntary Social Distancing
  • It should be noted that none of these researchers questioning the lockdown narrative express any problem with voluntary measures to reduce exposure to disease. Few are even likely to oppose measures like avoiding mass indoor gatherings.
  • But those sorts of measures are fundamentally different from mandated business closures and stay-at-home orders. The problem with mandatory lockdowns—in contrast to voluntary social distancing—is highlighted by the fact that they indiscriminately rob vulnerable populations of the services and assistance they need. And by “vulnerable populations” I mean anyone who is vulnerable to any life-threatening condition. Although we’re being conditioned to believe that deaths from covid are the only deaths worth noticing, the fact is that the world includes people who are vulnerable to suicide, to drug overdoses, and to economic ruin—which comes with countless secondary effects in the form of health problems. By denying these people the freedom to seek an income and secure the social and medical support they need, we are essentially saying that those people are expendable and it’s better to tilt the scales in favor of covid patients.
  • But as the mounting evidence discussed above suggests, the lockdowns don’t even produce the desired effects. So vulnerable people suffering from depression, untreated cancer, and other life-threatening conditions were forced to simply suffer unaided for no justifiable reason. This was done to fit a political narrative, but it was based on a batch of bad assumptions, half-baked science, and the arrogance of politicians.

Source:      https://www.zerohedge.com/covid-19/another-study-shows-yet-again-lockdowns-dont-work

L.      Practical Tips & Other Useful Information

1.      Depression and Stress Could Dampen Efficacy of C19 Vaccines: Interventions Could Boost Immunity 

  • Decades of research show that depression, stress, loneliness, and poor health behaviors can weaken the body’s immune system and lower the effectiveness of certain vaccines. A new report accepted for publication in Perspectives on Psychological Science suggests that the same may be true for the new C19 vaccines that are in development and the early stages of global distribution. Fortunately, it may be possible to reduce these negative effects with simple steps like exercise and sleep.
  • Vaccines are among the safest and most effective advances in medical history, protecting society from a wide range of otherwise devastating diseases, including smallpox and polio. The key to their success, however, is ensuring that a critical percentage of the population is effectively vaccinated to achieve so-called herd immunity.
  • Even though rigorous testing has shown that the C19 vaccines approved for distribution in the United States are highly effective at producing a robust immune response, not everyone will immediately gain their full benefit. Environmental factors, as well as an individual’s genetics and physical and mental health, can weaken the body’s immune system, slowing the response to a vaccine.
  • This is particularly troubling as the novel coronavirus continues to rage across the world, trigging a concurrent mental health crisis as people deal with isolation, economic stressors, and uncertainty about the future. These challenges are the same factors that have been previously shown to weaken vaccine efficacy, particularly among the elderly.
  • “In addition to the physical toll of C19, the pandemic has an equally troubling mental health component, causing anxiety and depression, among many other related problems. Emotional stressors like these can affect a person’s immune system, impairing their ability to ward off infections,” said Annelise Madison, a researcher at The Ohio State University and lead author on the paper. “Our new study sheds light on vaccine efficacy and how health behaviors and emotional stressors can alter the body’s ability to develop an immune response. The trouble is that the pandemic in and of itself could be amplifying these risk factors.”
  • Vaccines work by challenging the immune system. Within hours of a vaccination, there is an innate, general immune response on the cellular level as the body begins to recognize a potential biological threat. This frontline response by the immune system is eventually aided by the production of antibodies, which target specific pathogens. It is the continued production of antibodies that helps to determine how effective a vaccine is at conferring long-term protection.
  • “In our research, we focus most heavily on the antibody response, though it is just one facet of the adaptive immune system’s response,” said Janice Kiecolt-Glaser, director of the Institute for Behavioral Medicine Research at The Ohio State University and senior author on the paper.
  • The good news, according to the researchers, is that the C19 vaccines already in circulation are approximately 95% effective. Even so, these psychological and behavioral factors can lengthen the amount of time it takes to develop immunity and can shorten the duration of immunity.
  • “The thing that excites me is that some of these factors are modifiable,” said Kiecolt-Glaser. “It’s possible to do some simple things to maximize the vaccine’s initial effectiveness.”
  • Based on prior research, one strategy the researchers suggest is to engage in vigorous exercise and get a good night’s sleep in the 24 hours before vaccination so that your immune system is operating at peak performance. This may help ensure that the best and strongest immune response happens as quickly as possible.
  • “Prior research suggests that psychological and behavioral interventions can improve vaccine responsiveness. Even shorter-term interventions can be effective,” said Madison. “Therefore, now is the time to identify those at risk for a poor immune response and intervene on these risk factors.”

Source:      https://scitechdaily.com/depression-and-stress-could-dampen-efficacy-of-covid-19-vaccines-interventions-could-boost-immunity/

2.      Which masks are the most effective against new C19 strain?

  • French health honchos are urging citizens to say au revoir to cotton masks because they simply aren’t effective enough against new, potentially more contagious variants of C19.
  • Instead, France’s health advisory council has recommended that single-use surgical masks should be worn. Experts here agree — and tell The Post it’s an important time to consider upgrading your mask choice.
  • “As we progress in this pandemic, we are coming to the realization that no, not all masks are the same,” said Dr. Martin Cohen, assistant chair and teaching professor in the University of Washington’s Department of Environmental & Occupational Health Sciences. In the spring, he conducted crude aerosol experiments on masking materials to find suitable substitutes in the absence of personal protective equipment.
  • So which ones are the best? Here’s a look at which masks hold up in 2021 as scientists learn more about the increasingly mutating virus.
N95s
  • “The gold standard are obviously the N95 masks, regardless of the COVID strain,” said Dr. Rajesh Mohan, a New Jersey-based cardiologist.
  • It was also found to be the best mask in a comprehensive review of masks by Duke University researchers over the summer. 
  • It was the most effective of the bunch on the study’s logarithmic scale.
Surgical masks
  • Surgical masks, if replaced often, are the second-most effective type of mask to use in 2021.
  • Those single-use surgical masks are also a good standby, and considerably more comfortable than the face-conforming N95s.
  • “The next best thing is surgical masks,” Mohan said. “If people wore them, there would be about 70 percent decrease in infection.”
  • The Duke researchers also found it to be the second-most effective variety, ranging from 0 to 0.1 in terms of the particles spread from speaking while wearing one.
KN95s or KF94s
  • Aaron Collins, a Minnesota-based mechanical engineer, who wrote his master’s thesis on the science of aerosols and calls himself a “citizen scientist,” has been reviewing masks on his YouTube channel since August.
  • Collins turned his bathroom into a makeshift lab, using an aerosol generator to pump out tiny particles of salt and water. A condensation particle counter counts how many particles are in the air and how many are in the mask Collins is currently testing. He compares the number of particles inside the mask with the number outside it, which helps him determine its effectiveness.
  • His best bets, he found after his research, are protective masks such as KF94s, KN95s or N95s.
  • “N95s are obviously the best, because it seals to the face, but the disadvantage is that it is secured with a headband which can destroy your scalp.” In his research, he has found that KF94 masks range from 90 to 99% protection, while KN95 masks also perform well, but they have more variation in quality.
  • He advises against buying masks on eBay or Amazon because there are bootleg versions floating around.
  • Instead, he suggests buying from two companies: New Jersey-based importer Be Healthy USA and Bona Fide Masks.
Double masks
  • Two masks really are better than one as new variants of the coronavirus are found to be more contagious than previous variants.
  • Ever since November, when New England Patriots coach Bill Belichick wore two masks after his quarterback Cam Newton tested positive for C19, questions have swirled on whether doubling up is the best course of action.
  • “If your first line of protection is not significant, like a scarf, you can put on another layer,” said Mohan. Other researchers second that sentiment, saying a cloth mask and surgical mask make for an effective pairing.
  • “Obviously, the more layers you have of fibers between one person’s mouth and the other’s, there is less risk of spreading infection. But it could be diminishing the benefit, as far as the ability to breathe,” said Mohan. “The idea is that it should be snugly fit without making you uncomfortable.”

Source:      https://nypost.com/2021/01/21/the-most-effective-masks-against-the-new-covid-strain-experts/

3.        You Tested Positive for C19. Now What?

  • A C19 diagnosis can be unsettling and stir up anxiety and a flurry of questions. Many people who learn they have tested positive wonder how long they will be contagious, what they should or shouldn’t do while quarantining and when they can expect to see symptoms abate.
  • We asked doctors for answers to questions about dealing with a positive Covid test.
How long will I be contagious?
  • The U.S. Centers for Disease Control and Prevention says anyone who tests positive for C19 should isolate for 10 days starting at symptom onset. That means avoiding all contact with other people and not leaving home unless you need to go to a medical appointment. If you are asymptomatic and test positive and never develop symptoms, the isolation period should start on the day you took your diagnostic test. You are believed to no longer be contagious after 10 days if you have had no fever—and haven’t taken fever-reducing medication—for at least 24 hours and your symptoms are improving. The CDC recommends that immunocompromised patients and those with severe C19 cases isolate for up to 20 days after symptoms appear.
Do I need to tell people I’ve been in contact with that I tested positive?
  • Anyone who lives with you should get a C19 test and quarantine for 10 to 14 days from their last contact with you. In some cases quarantine can be shortened to seven days with a negative test. If you’ve spent a total of 15 minutes within 6 feet anyone else in the past two to four days, you should contact those people and let them know you tested positive. Some experts say if you are masked and outside there is significantly less risk and quarantine may not apply to those contacts, but it depends on the contact-tracing guidelines of your local health department.
  • “Public health authorities vary in advice,” says Graham Snyder, medical director of infection prevention and hospital epidemiology at the University of Pittsburgh Medical Center. “In our jurisdiction, if masked, we still consider yourself exposed if within 6 feet for 15 minutes. Obviously you’re less likely to be contagious or exposed if both people are masked and less likely to transmit virus if outdoors but there is a continuum where public health draws that line and it may vary.”
When I’m isolating, what can or can’t I do?
  • Isolation means avoiding all human contact as much as you can. Some cities and governments provide housing for people who need to isolate. If that’s not an option and you live with others, try to remain on your own floor or room with a private bathroom, if possible. Food and other essentials should be left outside your door. If someone enters your room or you need to venture out, make sure you are both masked. Some experts say walks aren’t allowed while in isolation. Others say as long as you are masked, feeling OK, and in an area where you can easily be very distant from others, it’s fine to go outside for fresh air.
Should I get another diagnostic test after my 10-day isolation period?
  • No. Many experts say that isn’t necessary and may result in unwarranted stress and anxiety should another test turn up positive. The PCR test commonly used to diagnose C19 is very sensitive and can detect virus particles that are dead or not infectious weeks later, says Kristin Englund, an infectious disease physician at Cleveland Clinic. “So it’s not going to be an accurate diagnosis of whether somebody is still infectious or not,” she says.
  • The only instance where a repeat diagnostic test may be necessary is for severely ill and immunocompromised patients whose recommended isolation period is up to 20 days following symptom onset.
What about an antibody test?
  • Doctors don’t recommend getting an antibody test in most cases. “Routine antibody testing after a Covid diagnosis is not necessary,” says Michael Lin, an infectious disease physician at Rush University Medical Center in Chicago. “It’s expensive and it does not change what you do day in and day out.”
  • Dr. Lin says, “We still don’t know if having a positive antibody test result means that you’re automatically protected or the converse, if a negative result means you’re at risk.” Doctors say it is important to observe pandemic protections after having had C19, including wearing a mask, social distancing and avoiding crowded, indoor spaces. A vaccine is still recommended so the results of an antibody test provide no useful information, they say.
  • The only reason someone might consider a test is if they were unable to get a diagnostic test but had C19 symptoms and want to see retroactively if that is in fact what they had, Dr. Lin says.
What if I don’t feel completely better after 10 days? If I’m still coughing do I have to worry about being contagious?
  • The CDC’s 10-day isolation recommendation relates to being contagious only. “The duration of symptoms doesn’t correlate with contagiousness,” says Dr. Snyder, of the University of Pittsburgh Medical Center. Many patients may feel fully recovered after 10 days or two weeks. But others may not be able to return to work and their normal routines. If your symptoms are improving and you don’t have a fever, that’s normal, he says.
  • “I don’t think you need to wait until you’re completely asymptomatic to come out of quarantine and to consider going back to normal daily activities,” says Dr. Englund. A recovery time of up to 28 days is reasonable, she says. After that, you should contact your primary care doctor.
What is long Covid?
  • Long Covid is a term for C19 patients who experience symptoms that can last for months after their initial acute Covid infection. Also called longhaulers, such patients often develop new and worsening symptoms even after recovering from their initial bout of Covid. Some patients were never hospitalized for acute C19 and are young and healthy with no underlying medical conditions. A recent study out of the United Kingdom’s Office of National Statistics estimated that 20% of Covid patients have symptoms for five weeks or longer and 10% have symptoms for 12 weeks or longer.
Can I get the C19 vaccine if I’ve had Covid and if so, how long do I have to wait?
  • Yes, you can and experts say you should get the vaccine as soon as you are eligible. Most people with C19 are thought to have some natural immunity and will be protected from getting the virus again for at least three months. “Theoretically the vaccine might boost immunity that a person has from being infected naturally,” says David Wohl, a professor of medicine in the division of infectious diseases at the University of North Carolina, Chapel Hill. There is no reason to wait, he says, except for ensuring that you are both outside the 10-day infectious period and fully recovered, since the vaccine can cause side effects or symptoms in some people.
Should I get the vaccine if I wasn’t hospitalized but had a monoclonal antibody treatment?
  • More outpatients are being treated now with the two monoclonal antibody treatments authorized for patients at risk of being hospitalized. Those patients should wait at least three months before getting the vaccine, says Dr. Wohl, because it takes the body several months to eliminate the antibodies and theoretically those antibodies could latch onto the proteins the vaccine teaches the body to make and hide them from the immune system.
Any symptoms that are a red flag to seek medical care?
  • Dr. Lin says during your active, acute infection if you feel short of breath and can’t speak in full sentences that is a sign your lungs are severely infected and you should seek medical care. Other red flag symptoms include confusion or signs of stroke, such as a sudden weakness in one part of your body or a loss of sensation. Dr. Lin says if you can’t do your daily activities after recovering from acute Covid, consult a doctor. [NOTE: As noted in previous Update editions, we highly recommend you purchase a pulse oximeter to monitor your oxygen levels, and to contact your health provider if your readings fall below 95%.]
When can I resume my normal exercise routine?
  • Experts say don’t jump right back into your fitness regimen if you were doing high-intensity exercise pre-Covid. “I would start back slowly,” says Dr. Wohl. “Listen to your body.” Even people who weren’t hospitalized may have inflammation in their lungs and not be exchanging oxygen the way they normally would, he says. Exercise as tolerated, Dr. Lin advises. “This particular virus has a propensity to infect the lungs,” he says. “So we do expect people to have potentially more trouble getting back to their normal exercise routine compared to other viruses.”
Any tests C19 patients should get to check for organ damage, like chest scans or electrocardiograms?
  • Experts don’t routinely recommend getting tests or scans unless there is a particular symptom that is lasting a long time and not improving, like shortness of breath or a racing heart beat.
Can C19 cause other dormant viruses, like the Epstein-Barr virus, which causes mononucleosis, or shingles to activate?
  • Yes. When the body is under stress, latent viruses can get reactivated. “In most cases those are transient increases in levels and don’t lead to any organ disease,” says Dr. Wohl. “We do know people when under stress or illness break out with other types of viruses, such as cold sores or even shingles.” Under such conditions, they can flare-up, he says.

Source:      https://www.wsj.com/articles/you-tested-positive-for-covid-19-now-what-11611579613

M.      Johns Hopkins COVID-19 Update

January 26, 2021

1.      Cases & Trends

Overview
  • The WHO C19 Dashboard reports 99.36 million cases and 2.14 million deaths as of 11am EST on January 26. The WHO reported decreasing global incidence for the second consecutive week, down to 4.10 million new cases last week, a 15.2% decrease from the previous week. But even with the recent decline, the average global daily incidence exceeds 575,000 new cases per day. At this pace, we expect the global cumulative incidence to surpass 100 million cases in the next 2 days. While daily incidence is decreasing, mortality continues to increase. The WHO reported 95,991 deaths last week, a new record and an increase of slightly more than 1% compared to the previous week.
  • Our World in Data reports that 55.58 million vaccine doses have been administered globally. 
United States
  • The US CDC reported 25.02 million total cases and 417,936 deaths. The US surpassed 25 million cumulative cases in yesterday’s update.
    • 1 case to 5 million cases- 200 days
    • 5 million to 10 million- 92 days
    • 10 million to 15 million- 29 days
    • 15 million to 20 million- 24 days
    • 20 million to 25 million- 23 days

2.      AUSTRALIA VACCINE AUTHORIZATION 

  • On January 25, the Australian Therapeutic Goods Administration granted provisional authorization for the use of the Pfizer/BioNTech vaccine candidate. The provisional approval applies for use in individuals aged 16 years and older, and vaccinations are expected to begin in February. Australian Prime Minister Scott Morrison emphasized that the provisional approval is different from an emergency authorization and requires a more comprehensive review of the vaccine’s safety and efficacy, among the first such effort globally. The vaccine will be provided for free to all Australian citizens. According to the National Rollout Strategy, as many as 1.4 million doses will be distributed to “1a” priority groups, which include healthcare workers, long-term care facility staff and residents, and border and quarantine workers. The vaccine will initially be delivered to 50 priority vaccination sites during Phase 1a and then expanded to more than 1,000 sites nationwide. The initial vaccine hubs are concentrated in coastal areas, where the majority of the population resides. Few of the initial sites are located in Australia’s interior where many aboriginal communities reside. Australian authorities must set up cold storage facilities and train vaccinators in advance of beginning Phase 1a, and each batch will be tested before doses are administered.

3.      VACCINE DONATIONS 

  • India has pledged to donate more than 4.5 million doses of the AstraZeneca vaccine, manufactured in India by the Serum Institute, to several neighboring countries. Deliveries have reportedly already arrived in Bangladesh, Bhutan, Maldives, Mauritius, Nepal, and Seychelles, and additional donations are expected for Afghanistan and Sri Lanka. India has already stockpiled 80 million doses of the AstraZeneca vaccine, and it is expected to manufacture an additional 50 million doses per month. In addition to India, China has donated vaccine to numerous countries, including Myanmar, Cambodia, Philippines, and Pakistan. Commentators have noted that these donations may be a strategic form of diplomacy that aims, in part, to increase political influence in the region and improve bilateral relations. In addition to donations, both India and China have also sold doses of vaccine to global partners. 

4.      US TRAVEL RESTRICTIONS 

  • Yesterday, US President Joe Biden issued travel restrictions for several countries that are currently experiencing increased C19 incidence, including several emerging variants of SARS-CoV-2. The restrictions apply to individuals who traveled to Brazil, Ireland, South Africa, the UK, or any country in the EU (Schengen Area) in the 14 days prior to their arrival in the US. The restrictions existed previously for Brazil, Ireland, the UK, and the EU, but South Africa is new to the list. The presidential proclamation took effect today. Dr. Anthony Fauci described the restrictions as “very prudent,” particularly as new evidence indicates that these emerging variants may be associated with increased mortality risk. Exceptions to the new policy include US citizens, permanent residents, noncitizen nationals, certain immediate family members of permanent residents or citizens, individuals who fall under exceptions related to US national interests and individuals seeking asylum.

5.      MEXICAN PRESIDENT 

  • On Sunday, Mexican President Andrés Manuel López Obrador announced that he tested positive for SARS-CoV-2. President Obrador described his symptoms as “mild,” but he is currently undergoing medical treatment. President Obrador will continue to isolate at home, and he has handed off responsibility for daily news conferences to Mexico’s Secretary of the Interior, Olga Sánchez Cordero. President Obrador had not yet been vaccinated against SARS-CoV-2.

6.      RESTRICTIONS & PROTESTS 

  • For the past several days in the Netherlands, protests against stronger C19 restrictions have turned violent. The Dutch government implemented new ”lockdown measures” on January 23, including a nighttime curfew from 8:30pm-4:30am, a travel advisory discouraging any travel out of the country, and a limit of 1 visitor per household per day. The curfew, in particular, drew opposition from the public. As we covered previously, the last time that the Netherlands implemented a nationwide curfew was during World War II. The large public protests turned violent on Sunday the 24, reportedly including a fire at a SARS-CoV-2 testing center. Since then, hundreds of protestors have been arrested, and several cities have imposed ordinances against entering the city center in order to suppress further riots. Prime Minister Mark Rutte condemned the riots, describing the events as instances of criminal violence rather than protests. The curfew and other new measures are scheduled to remain in place through February 9. 

7.      ECONOMIC IMPACT & RECOVERY 

  • A report published this week by Oxfam International illustrates significant disparities in terms of the financial impact of the C19 pandemic. The report—released to coincide with the annual World Economic Forum summit typically held in Davos, Switzerland—indicates that the “mega-rich” have already recovered financially from the pandemic, whereas the world’s poorest could take years or longer. Notably, the research suggests that C19 could exacerbate economic inequalities in nearly every country on Earth. The 1,000 wealthiest people in the world, “mostly White male[s],” took approximately 9 months to recuperate financial losses, but those living in poverty are expected to take more than a decade to recover. The analysis also estimates that “the increase in the 10 richest billionaires’ wealth since the crisis began [more than US$500 billion] is more than enough to prevent anyone on Earth from falling into poverty because of the virus, and to pay for a C19 vaccine for everyone.” Notably, women and racial and ethnic minorities are disproportionately affected by the global economic crisis. In addition to shorter-term and immediate financial struggles, many people around the world will face prolonged financial hardship stemming from the pandemic, compounding economic inequalities around the world.
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