Coronavirus Update

Without reliable information, we rely on fear or luck.

Coronavirus Update 10-15

Thursday Edition

October 15, 2020

Without reliable information, we rely on fear or luck.

“This was a way for me to take back control of the situation, to feel like I was in a less hopeless place, and a less hopeless world, and be like, OK, I can do this. To make it better, I chose not to be in fear.” 

Estefania Hidalgo, 32, a British photography student who works at a gas station and a challenge trial volunteer

“Slightly more than half of Americans say they already have or plan to stockpile food and other essentials. The chief reason: fears of a resurgent pandemic, which could lead to disruptions such as new restrictions on businesses. On Oct. 2, the number of COVID-19 cases in the USA was its highest in almost two months.”  

Poll byScience and Leisure Group

Index

A. The Pandemic As Seen Through Headlines

B. Numbers & Trends

1. Cases & Tests

2. Deaths

3. Top 5 States in Cases, Deaths, Hospitalizations & Positivity 

4. Trouble on both sides of the Atlantic

5. A dose of optimism

6. But some chaos still lies ahead

C. New Scientific Findings & Research

1. Stopping C19 by targeting out-of-control immune cells  

2. Age does not contribute to C19 susceptibility  (!)

3. Total deaths during the pandemic far exceed those attributed to C19  

4. New Evidence of Link Between Blood Type & C19 Susceptibility 

5. Supercomputer shows how humidity affects spread of C19  (*)

6. The Coronavirus Unveiled  

7. C19 can survive up to 28 days on surfaces  

 D. Vaccines & Testing

1. More than 30,000 Sign Up To Be Infected With C19 To Test Experimental Vaccine 

2. Positive Preliminary Results for 30 Second Rapid Test  

3. Abbott’s coronavirus antibody test gets FDA’s emergency use approval  

E. Improved & Potential Treatments

1. Anti-ageing drugs could make C19 vaccines more effective in older people  

2. Lab-Made ‘Miniproteins’ Could Block C19 from Infecting Cells  (!)

3. Study to test whether vitamin D can protect people from C19   

4. The other race for a virus treatment

F. Concerns & Unknowns

1. Staggering 86% who tested Covid positive in lockdown had NONE of the official symptoms   (!)

2. COVID-related delays to colorectal cancer screening causing 11.9% rise in death rates  (*)

3. C19 can infect your eyes as well as your lungs  

4. If You Have This BMI Your Risk of COVID Death Increases  (*)

5. Hearing Loss is a potential symptom of C19  

6. A man caught coronavirus twice—and it was worse the second time  

G. Projections & Our (Possible) Future

1. More Than Half Of All Americans “Plan To Stockpile Food And Other Essentials” For The Chaotic Months Ahead   (*)

H. Lockdowns

1. Swedish Health Chief Said Country Avoided Lockdown To Prevent “Pandemic Fatigue”  

2. Making Sense of Sweden  

I. Johns Hopkins COVID-19 Update 

J. Linked Stories

1. Scientists have a powerful new tool for controlling the coronavirus: Its own genetic code  

2. Pandemic-related stress leads to less employee engagement

3. New study suggests crucial role for lymphocytes (especially T cells) in asymptomatic C19 infection 

4. Immune System’s Response to C19 Was Just Revealed by Scientists Who Discovered SARS  

5. New blood test predicts which C19 patients will develop severe infection  

6. Could an existing vaccine make C19 less deadly? Mexico City study provides support  

7. NIH study aims to identify promising C19 treatments for larger clinical trials  

8. Combining Rapid PCR and Antibody Tests Improved C19 Diagnosis

Notes:

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  • We do not endorse, and may not agree with, any opinion or view included in this update.  We include a wide spectrum of opinions and views as we believe that it gives perspective on what people are thinking and may give insights into our future.

A. The Pandemic As Seen Through 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 = 38,730,280
  • New Cases = 381,446
  • New Cases (7 day average) = 334,156 (+5,323) (+1.6%)
Observations:
  • Number of new cases is a record high
  • 7 day average of new cases is a record high
US Cases & Testing: 
  • Total Cases = 8,150,043
  • New Cases = 59,693
  • Percentage of New Global Cases =  15.6%    
  • New Cases (7 day average) = 53,151 (+1,474) (+2.9%)
  • Total Number of Tests = 121,567,138
  • Percentage of positive tests (7 day average) = 5.9%
Observations:
  • 7 day average of new cases has been mostly increasing since 9/12, and has been increasing rapidly since 10/2
  • Percentage of positive tests (7 day average) has been steadily increasing since 9/29
  • Recent increases in 7 day average of new cases and percentage of positive tests are a worrisome trend and could foreshadow an increase in deaths in the near future

2. Deaths

Worldwide Deaths: 
  • Total Deaths = 1,096,323
  • New Deaths = 6,083
  • New Deaths (7 day average) = 5,189 (+25) (+0.5%)
Observations:
  • Although 7 day average is up slightly, the 7 day average has mostly been trending lower since 2nd peak on 8/11
US Deaths: 
  • Total Deaths = 221,843
  • New Deaths = 970
  • Percentage of Global New Deaths = 15.9%
  • New Deaths (7 day average) = 723 (+6) (+0.9%)
Observations:
  • 7 day average of new deaths has been within a between 770 and 717 deaths since 9/21, a range of approx. 7%
  • 7 day average has decreased from 1,178 to 723 since 2nd peak on 8/4, a decrease of 38.6% 

3. Top 5 States in Cases, Deaths, Hospitalizations & Positivity (10/14)

ChartChart
ChartChart
Observations:
  • While TX hit its highest daily case count since 10/3 (7,006 new cases), its 7-day average cases have decreased 6.3% over the same 7-day average from two weeks ago (9/30)
  • ND and SD positivity rates are both above 30%. This is the first day in which the SD 7-day positivity rate has been above 30%. ND’s positivity rate first reached 30% on 9/25. ND hospitalizations have increased 131% to 206 patients while SD hospitalizations have increased 43% to 303 patients. 
  • The overall positivity rate for the US has increased to 5.9%. On 9/29, the positivity rate was 4.9% which was the lowest level since it reached 4.8% on 6/18

4. Trouble on both sides of the Atlantic

  • From Milwaukee to Moscow, from Boston to Barcelona, startling fall surges in coronavirus cases are quickly filling hospital beds, threatening fresh lockdowns in Europe and the United States and potentially setting the stage for wintertime peaks.
  • In the U.S., new cases are rising in 39 states, and the country is registering its highest curve of new cases since August. Hot spots are cropping up in the Northeast, which is starting to backslide after months of progress, and uncontrolled outbreaks in the Northern Plains and the Mountain West are straining hospitals.
  • Even with testing still insufficient in much of the country, 16 states added more new cases last week than they had in any other weeklong stretch of the pandemic. North Dakota and South Dakota are reporting more new cases per capita than any other states to date.
  • Across the country, 36,051 people were hospitalized with C19 as of Tuesday evening, a higher number than at any time since Aug. 29, according to the Covid Tracking Project.
  • There is also growing concern about the damage a winter wave could sow in the formerly Communist countries of Central Europe, which have weak health care systems, critical shortages of doctors and nurses and some of the highest transmission rates in Europe.
  • For weeks, European leaders have desperately tried to avoid reimposing economically damaging lockdowns, opting instead for the lightest possible measures. However, the current wave is now forcing fresh containment measures — bars and clubs have been shuttered in Prague and pubs and gyms closed in Liverpool, and masks are now mandatory in public indoor spaces in Amsterdam. Northern Ireland will lock down for four weeks.
  • In the most vivid sign of the deteriorating situation, President Emmanuel Macron of France declared a state of emergency today and said he would impose a curfew of 9 p.m. to 6 a.m. in the Paris region and eight other major metropolitan areas, beginning on Saturday.
  • “The virus is everywhere in France,” he said.

Source: New York Times Coronavirus Briefing

5. A dose of optimism

  • Our colleague Donald G. McNeil Jr. wrote that since January, when he began covering the coronavirus, he has been a “consistently gloomy Cassandra” — reporting on the catastrophic fallout of the pandemic that many experts saw coming.
  • And yet, he said, he has recently become cautiously optimistic.
  • The worst-case scenario — in which some 2.2 million Americans die from the virus — has not come to pass. Around the world, hundreds of millions of people have made huge sacrifices in shutting down parts of the economy, maintaining social distance and wearing masks.
  • Those sacrifices have made the possibility of a “twindemic” of coronavirus and influenza infections seem far less likely now, too. The flu season is typically seeded each year in the Northern Hemisphere by travelers from the Southern Hemisphere. But this year the flu season there was almost nonexistent because of anti-coronavirus measures.
  • Donald also noted that the percentage of infected people who are dying from the virus has been falling because of all of the lessons we’ve learned during the last few months. Nursing homes have gotten better at protecting their residents, steroids like dexamethasone have lowered the number of deaths, and tactics like rolling patients onto their stomachs and delaying ventilator use have also been shown to help. Pharmaceutical interventions like monoclonal antibodies, still in the early stages of availability, are likely to become even more effective.
  • Vaccine development has been moving much faster than anticipated in part because the Trump administration’s Operation Warp Speed appears to be working. It has put more than $11 billion into seven vaccine candidates, and Moncef Slaoui, the chief scientific adviser on the program, said he expected two to be approved by January, with an efficacy of 75 to 90%. Mr. Slaoui also said that factories would produce enough doses for all 330 million Americans to be vaccinated by next June. That all suggests the pandemic in the United States may be over far sooner than expected, possibly by the middle of next year.
  • Still, we’re not there yet — and the pandemic has repeatedly taken a turn for the worse just when things were looking better. Cases are still on the rise in most of the United States and across the world, and experts warn that autumn and winter may be grim as indoor dining, in-school instruction, jet travel and family holidays end up increasing infections, hospitalizations and deaths.
  • “Pandemics don’t end abruptly; they decelerate gradually, like supertankers,” Donald wrote. “Even by spring, we will not be entirely safe, but we probably will be safer.”

Source: New York Times Coronavirus Briefing

6. But some chaos still lies ahead

  • Many leaders — most notably President Trump — have described the arrival of a coronavirus vaccine as an off switch that will instantly normalize our lives. But experts are warning of a perplexing and frustrating period that could follow.
  • Our colleague Carl Zimmer wrote that when the first vaccine arrives, it may not be the most effective vaccine, offering only moderate protection that will make it prudent to keep wearing a mask.
  • And the first vaccine to reach the finish line may end up hampering the trials of its competitors.
  • Volunteers in experimental trials may drop out, slowing down research and regulatory approval. And vaccines that are not as far along might have to prove that they are better than the first shot, resulting in trials that are bigger and take more time. That could lead to steep costs that may halt development.
  • One possibility: By next spring or summer, there could be a number of vaccines on the market without a clear sense of how to choose among them.
  • Some of this confusion is inevitable, but it’s also a result of how the process was designed. Rather than testing a number of vaccines against each other, as the World Health Organization is doing, the United States took a “harmonized approach” that allowed vaccine companies to run their own trials as long as they followed certain guidelines.
  • Finally, drug companies and regulators will have to monitor patients, even after clinical trials are over, to look for rare but dangerous side effects. Random events — like a group of older people all having strokes shortly after being vaccinated — could raise the possibility that the vaccine was the culprit. The uncertainty may lead some people to avoid vaccines entirely, which would weaken our collective ability to fight C19.

Source: New York Times Coronavirus Briefing

C. New Scientific Findings & Research

1. Stopping C19 by targeting out-of-control immune cells  

  • The coronavirus (SARS-CoV-2) prompts the immune system to attack healthy cells, leading to dangerous inflammation. But how does the virus enable this attack? Johns Hopkins University researchers have taken one step toward answering that question—and suggested a potential solution in drugs that are already in clinical testing.
  • The Johns Hopkins team focused on two proteins, factor H and factor D, which are known as “complement” proteins, because they help the immune system clear pathogens from the body. The researchers discovered that C19’s spike protein causes factor D to overstimulate the immune response, which in turn prevents factor H from mediating that response. Blocking factor D prevents that chain of events, they reported in the journal Blood.
  • Previous studies had shown that C19 “activates a cascading series of biological reactions—what we call the alternative pathway of complement,” said senior author Robert Brodsky, M.D., director of the hematology division at the Johns Hopkins University School of Medicine, in a statement. “The goal of our study was to discover how the virus activates this pathway and to find a way to inhibit it before the damage happens.”
  • The researchers zeroed in on a process that occurs when the spike protein binds to healthy cells: The spikes attach to a sugar molecule called heparan, which is prevalent on cells in the lungs, blood vessels and organ muscles. They discovered that during that process, SARS-CoV-2 blocks factor H from binding to cells, leaving them vulnerable to the dangerous immune attack.
  • Because factor D is upstream in the complement pathway, the researchers figured that blocking it might stop that immune response. They tested a small-molecule factor D inhibitor, ACH-145951, in cells and found that SARS-CoV-2’s spike protein was unable to activate the alternative complement pathway, they reported.
  • Factor D inhibitors are being developed by the likes of Alexion to address complement alternative pathway-mediated diseases. And Alexion launched a phase 3 trial of a different complement-directed drug, Ultomiris, in severe C19 patients in April. Ultomiris works by inhibiting “terminal” complements and is approved by the FDA to treat rare blood disorders.
  • Also this week, a team of researchers at Imperial College London reported their discovery that another protein, Foxp3, plays a role in mediating the inflammatory immune response to C19. They explained the findings in the journal Frontiers in Immunology.
  • They studied tissue samples from the lungs of six severely ill patients, three moderately sick patients and three healthy people in China. The researchers discovered that the lungs of the sickest C19 patients were filled with “hyperactive” T cells, suggesting a failure of the braking mechanism in the immune system that prevents dangerous immune reactions, they said in a statement. Foxp3 usually initiates that braking system but was lacking in the samples from those patients.
  • The Imperial College team is now planning future studies aimed at better understanding Foxp3’s role in C19 and finding ways to restore the immune system’s braking mechanism.

Source: Stopping COVID-19 by targeting out-of-control immune cells 

2. Age does not contribute to C19 susceptibility  

  • Scientists have estimated that the age of an individual does not indicate how likely they are to be infected by the coronavirus (SARS-CoV-2). However, development of symptoms, progression of the disease, and mortality are age-dependent.
  • There have been a large number of deaths due to the ongoing C19 pandemic, and it has been shown that elderly individuals disproportionately develop severe symptoms and show higher mortality.
  • A team of scientists, including Associate Professor Ryosuke Omori from the Research Center for Zoonoses Control at Hokkaido University, have modeled available data from Japan, Spain and Italy to show that susceptibility to C19 is independent of age, while occurrence of symptomatic C19, severity and mortality is likely dependent on age. Their results were published in the journal Scientific Reports on October 6, 2020.
  • Causes of mortality in elderly individuals may be due to two factors: how likely they are to be infected due to their advanced age (age-dependent susceptibility), which is reflected in the number of cases; and, how likely they will be affected by a severe form of the disease due to their advanced age (age-dependent severity), which is reflected in the mortality rate. These factors are not fully understood for C19.
  • The scientists chose to analyze data from Italy, Spain and Japan to determine if any relationship between age, susceptibility and severity. These three countries were chosen as they have well recorded, publicly available data. As of May 2020, the mortality rate (number of deaths per 100,000) was 382.3 for Italy, 507.2 for Spain and 13.2 for Japan. However, despite the wide disparity in mortality rates, the age distribution of mortality (the proportional number of deaths per age group) was similar for these countries.
  • The scientists developed a mathematical model to calculate susceptibility in each age group under different conditions. They also factored in the estimated human-to-human contact level in each age group, as well as varying restriction levels for outside-home activities in the three countries.
  • The model showed that the susceptibility has to be unrealistically different between age groups if they assume age does not influence severity and mortality. On the other hand, the model indicated the age should not influence susceptibility but should negatively influence severity and mortality, to explain the fact that the age distribution of mortality is similar between the three countries.
  • Ryosuke Omori, from the Research Center for Zoonoses Control at Hokkaido University, specializes in epidemiological modelling: the use of mathematics and statistics to understand and predict the spread of diseases. Since the outbreak of C19, he has turned his efforts to ascertaining the true extent of the spread of the pandemic in Japan and abroad.

Source: Age does not contribute to COVID-19 susceptibility

3. Total deaths during the pandemic far exceed those attributed to C19  

  • For every two deaths attributed to C19 in the U.S., a third American dies as a result of the pandemic, according to new data publishing Oct. 12 in the Journal of the American Medical Association.
  • The study, led by researchers at Virginia Commonwealth University, shows that deaths between March 1 and Aug. 1 increased 20% compared to previous years — maybe not surprising in a pandemic. But deaths attributed to C19 only accounted for 67% of those deaths.
  • “Contrary to skeptics who claim that C19 deaths are fake or that the numbers are much smaller than we hear on the news, our research and many other studies on the same subject show quite the opposite,” said lead author Steven Woolf, M.D., director emeritus of VCU’s Center on Society and Health.
  • The study also contains suggestive evidence that state policies on reopening early in April and May may have fueled the surges experienced in June and July.
  • “The high death counts in Sun Belt states show us the grave consequences of how some states responded to the pandemic and sound the alarm not to repeat this mistake going forward,” said Woolf, a professor in the Department of Family Medicine and Population Health at the VCU School of Medicine.
  • Total death counts in the U.S. are remarkably consistent from year to year, as the study notes. The study authors pulled data from the Centers for Disease Control and Prevention for 2014 to 2020, using regression models to predict expected deaths for 2020.
  • The gap between reported C19 deaths and all unexpected deaths can be partially explained by delays in reporting C19 deaths, miscoding or other data limitations, Woolf said. But the pandemic’s other ripple effects could explain more.
  • “Some people who never had the virus may have died because of disruptions caused by the pandemic,” said Woolf, VCU’s C. Kenneth and Dianne Wright Distinguished Chair in Population Health and Health Equity. “These include people with acute emergencies, chronic diseases like diabetes that were not properly care for, or emotional crises that led to overdoses or suicides.”
  • For example, the study specifically showed that the entire nation experienced significant increases in deaths from dementia and heart disease. Woolf said deaths from Alzheimer’s disease and dementia increased not only in March and April, when the pandemic began, but again in June and July when the C19 surge in the Sun Belt occurred.
  • This study, with data from March to Aug. 1, builds on a previously published JAMA article by the same authors from VCU and Yale University that focused on data from March to May 1. And it brings in new data about the timing of when states lifted restrictions on social distancing.
  • States like New York and New Jersey, which were hit hard early, were able to bend the curve and bring death rates down in less than 10 weeks. Meanwhile, states such as Texas, Florida and Arizona that escaped the pandemic at first but reopened early showed a protracted summer surge that lasted 16-17 weeks — and was still underway when the study ended.
  • “We can’t prove causally that the early reopening of those states led to the summer surges. But it seems quite likely,” said Woolf. “And most models predict our country will have more excess deaths if states don’t take more assertive approaches in dealing with community spread. The enforcement of mask mandates and social distancing is really important if we are to avoid these surges and major loss of life.”
  • Woolf paints a grim picture, warning that long-term data may show a broader impact of the pandemic on mortality rates. Cancer patients who have had their chemotherapy disrupted, women who have had their mammograms delayed — preventable, early deaths may increase in the coming years, he said.
  • “And death is only one measure of health,” Woolf said. “Many people who survive this pandemic will live with lifelong chronic disease complications. Imagine someone who developed the warning signs of a stroke but was scared to call 9-1-1 for fear of getting the virus. That person may end up with a stroke that leaves them with permanent neurological deficits for the rest of their life.”
  • Diabetes complications that aren’t being managed properly could lead to kidney failure and dialysis. And behavioral health issues, like emotional trauma, are going untreated. Woolf worries most about the lasting effects on children — long-term, generational outcomes.
  • “This isn’t a pandemic involving a single virus,” said Peter Buckley, M.D., dean of the VCU School of Medicine. “This is a public health crisis with broad and lasting ripple effects. VCU researchers have been diligent in their investigations into both treatment of C19 and in understanding the long-term repercussions of the pandemic, so that fellow doctors, policymakers and community members can fight these battles on multiple fronts.”

Source: Total deaths recorded during the pandemic far exceed those attributed to COVID-19

4. New Evidence of Link Between Blood Type & C19 Susceptibility 

  • Two new studies suggest people with blood type O may have a lower risk of C19 infection and reduced likelihood of severe outcomes, including organ complications, if they do get sick.
  • These new studies add evidence that there may be an association between blood type and vulnerability to C19; however, additional research is needed to better understand why and what it means for patients.
Individuals with blood type O may be less vulnerable to C19 infection
  • Blood type O may offer some protection against C19 infection, according to a retrospective study . Researchers compared Danish health registry data from more than 473,000 individuals tested for C19 to data from a control group of more than 2.2 million people from the general population. Among the C19 positive, they found fewer people with blood type O and more people with A, B, and AB types.
  • The study results suggest that people with blood types A, B, or AB may be more likely to be infected with C19 than people with type O. The researchers did not find any significant difference in rate of infection between A, B, and AB types. Since blood group distributions vary among ethnic subgroups, the researchers also controlled for ethnicity and maintained that fewer people with blood type O tested positive for the virus.
  • “It is very important to consider the proper control group because blood type prevalence may vary considerably in different ethnic groups and different countries,” said study author Torben Barington, MD, of Odense University Hospital and the University of Southern Denmark. “We have the advantage of a strong control group – Denmark is a small, ethnically homogenous country with a public health system and a central registry for lab data – so our control is population-based, giving our findings a strong foundation.”
  • People with blood groups A or AB appear to exhibit greater C19 disease severity than people with blood groups O or B, according to a separate retrospective study. Researchers examined data from 95 critically ill C19 patients hospitalized in Vancouver, Canada. They found that patients with blood groups A or AB were more likely to require mechanical ventilation, suggesting that they had greater rates of lung injury from C19. They also found more patients with blood group A and AB required dialysis for kidney failure.
  • Together, these findings suggest that patients in these two blood groups may have an increased risk of organ dysfunction or failure due to C19 than people with blood types O or B. Furthermore, while people with blood types A and AB did not have longer overall hospital stays than those with types O or B, they did remain in the intensive care unit (ICU) for a longer average time, which may also signal a greater C19 severity level.
  • “The unique part of our study is our focus on the severity effect of blood type on C19. We observed this lung and kidney damage, and in future studies, we will want to tease out the effect of blood group and C19 on other vital organs,” said study author Mypinder S. Sekhon, MD, of the University of British Columbia. “Of particular importance as we continue to traverse the pandemic, we now have a wide range of survivors who are exiting the acute part of C19, but we need to explore mechanisms by which to risk stratify those with longer-term effects.”

Source: New Evidence of Link Between Blood Type & COVID-19 Susceptibility

5. Supercomputer shows how humidity affects spread of C19  

  • A Japanese supercomputer has shown how humidity affects the spread of viral particles – suggesting that the use of humidifiers may help limit coronavirus infections during dry conditions this winter, according to a report.
  • Researchers used Fugaku supercomputer to illustrate the emission and spread of virus-like particles from infected people in a range of indoor environments, Reuters reported.
  • Humidity of less than 30% resulted in more than double the amount of aerosolized particles compared to levels of 60% or greater, according to the simulations by research giant Riken and Kobe University.
  • Watch a video of the study here: https://youtu.be/4TUrsRvKZOc 
  • The study also found that clear face shields are not as effective as masks in preventing the spread of aerosols and that diners are more at risk from people to their side compared to across the table.
  • There has been a growing consensus among health experts that the deadly bug can be spread through the air. The Centers for Disease Control and Prevention recently revised its guidance to say the pathogen can linger in the air for hours.
  • The Riken research team led by Makoto Tsubokura has previously used the supercomputer to study contagion conditions in trains, work spaces, and classrooms.
  • The simulations showed that opening windows on trains can increase the ventilation by two to three times, lowering the concentration of microbes.
  • “People’s blind fear or unfounded confidence against the infection of C19 is simply because it is invisible,” Tsubokura said.

Source: Supercomputer shows humidity affects spread of coronavirus

6. The Coronavirus Unveiled  

  • In February, as the new coronavirus swept across China and shut down entire cities, a scientist named Sai Li set out to paint its portrait.
  • At the time, the best pictures anyone had managed to take were low-resolution images, in which the virus looked like a barely discernible smudge.
  • Dr. Li, a structural biologist at Tsinghua University in Beijing, joined forces with virologists who were rearing the virus in a biosafety lab in the city of Hangzhou. Those researchers doused the viruses with chemicals to render them harmless and then sent them to Dr. Li.
  • Dr. Li and his colleagues then concentrated the virus-laden fluid from a quart down to a single drop. He could only hope that they had done everything just right, so that the weeks of work to produce that drop would not have been a waste.
  • “At the time, you don’t know what’s inside,” Dr. Li said. “It’s just liquid, right?”
Glimpsing the Structure
  • Dr. Li carefully froze the drop in a fraction of a second. If he made the slightest mistake, ice crystals could spear the viruses, tearing them apart.
  • Hoping for the best, Dr. Li placed the smidgen of ice into a cryo-electron microscope. The device fired beams of electrons at the sample. As they bounced off the atoms inside, Dr. Li’s computer reconstructed what the microscope had seen. When the picture formed, he was taken aback.
  • “I saw a screen full of viruses,” Dr. Li recalled.
  • He could see thousands of coronaviruses packed in the ice like jellybeans in a jar. They were beautifully intact, allowing him to inspect details on the viruses that measured less than a millionth of an inch.
  • “I thought, I was the first guy in the world to see the virus in such good resolution,” Dr. Li recalled.
  • Over the following weeks, Dr. Li and his colleagues pored over the viruses. They inspected the proteins that studded its surface and they dove into its core, where the virus’s strand of genes was coiled up with proteins. The pictures reminded Dr. Li of eggs in a nest.
  • Thanks to the work of scientists like Dr. Li, the new coronavirus (SARS-CoV-2) is no longer a cipher. They have come to know it in intimate, atomic detail. They’ve discovered how it uses some of its proteins to slip into cells and how its intimately twisted genes commandeer our biochemistry. They’ve observed how some viral proteins throw wrenches into our cellular factories, while others build nurseries for making new viruses. And some researchers are using supercomputers to create complete, virtual viruses that they hope to use to understand how the real viruses have spread with such devastating ease.
  • “This time is unlike anything any of us has experienced, just in terms of the bombardment of data,” said Rommie Amaro, a computational biologist at the University of California at San Diego.
Probing the Spike
  • Earlier this year, Dr. Amaro and other researchers directed much of their attention to the proteins, called spikes, that stud the virus’s surface. Spike proteins have an essential job to play: They latch onto cells in our airway so the virus can slip inside. But it soon became clear that the name is a misnomer. The spike protein is not sharp, narrow or rigid.
  • Each spike protein snaps together with two others, forming a structure that has a tulip-like shape. A long stem anchors the proteins to the virus, and their top looks like a three-part flower.
  • Gerhard Hummer, a computational biophysicist at the Max Planck Institute of Biophysics, and his colleagues used the frozen microscopy method to take pictures of spike proteins embedded in the virus membrane. Then they calculated how the atoms in the proteins pushed and pulled on each other. The result was a molecular dance: The spike proteins swivel around on three hinges.
  • “You can see these flowers waving with all kinds of bending angles,” Dr. Hummer said. “It’s quite surprising to have such a long, slender stalk with so much flexibility.”
A Sugar Shield
  • Dr. Hummer speculated that the flexibility of the spike was important to the virus’s success. By sweeping around, the spike increases its odds of encountering the protein on the surface of our cells it uses to attach.
  • As they sweep around, however, the spikes can be attacked by antibodies, the powerful soldiers of our immune system. To hide, they create a shield out of sugar. Sugar molecules, in navy below, swirl around the proteins and hide them from antibodies.
  • A little hook at the end of the spike protein, in light blue below, sometimes flips up above the sugar shield. If it encounters a particular protein on the surface of our cells, it sets off a series of reactions that allows the virus to fuse to a cell membrane and inject its genes.
Tangled Loops
  • The genes of the new coronavirus are arrayed on a molecular strand called RNA. On Jan. 10, Chinese researchers published its sequence of 30,000 letters. That genetic text stores the information required for a cell to make the virus’s proteins.
  • But the genome is more than a cookbook. The strand folds into a devilishly complex tangle. And that tangle is crucial for the virus’s exploitation of our cells. “You have a lot more information stored in how it’s shaped,” said Sylvi Rouskin, a structural biologist at the Whitehead Institute.
  • Dr. Rouskin led a team of scientists who mapped that shape. In a high-security lab at Boston University, her colleagues infected human cells with the viruses and gave them time to make thousands of new RNA strands. Tagging the genetic letters on the strands with chemicals, Dr. Rouskin and her colleagues could determine how the strand folded in on itself.
  • In some places it only formed short side-loops. In other places, hundreds of RNA letters ballooned out into big hoops, with loops coming off, and more loops coming off of them. By comparing millions of viral genomes, Dr. Rouskin and her colleagues discovered places where the virus slips from one shape to another.
  • A number of researchers are now closely examining some of these regions to figure out what they’re doing. Their studies suggest that these knots allow the virus to control our ribosomes, the tiny cellular factories that pump out proteins.
  • After the virus enters a human cell, our ribosomes attach to its RNA strands and glide down them like a roller coaster car running along a track. As the ribosomes pass over the genetic letters, they build proteins with corresponding structures. Scientists suspect that the loops of RNA may throw the roller coaster car off its track and then guide it to a spot thousands of positions away.
  • Other loops force the ribosome to back up a bit and then move forward again. This little hiccup can cause the virus to make entirely different proteins from the same stretch of RNA.
Jamming the Machinery
  • The viral proteins that spew out of our ribosomes fan out across the cell to carry out different tasks. One of them, called Nsp1, helps seize control of our molecule machinery.
  • Joseph Puglisi, a structural biologist at Stanford, and his colleagues mixed Nsp1 proteins and ribosomes together in test tubes. They found that the proteins, in pink below, slipped neatly into the channels inside the ribosomes where RNA would normally fit.
  • Dr. Puglisi suspects that Nsp1 stops our cells from making proteins of their own — especially the antiviral proteins that could destroy the virus. But that raises the question of how the virus gets its own proteins made.
  • One possibility is that “somehow the virus is just amped up in its ability to produce protein,” Dr. Puglisi said. From time to time, Nsp1 falls out of ribosomes, and somehow the virus does a better job of taking advantage of those brief opportunities. “We hoped it was going to be something simple,” he said. “But, as usual in science, it wasn’t.”
Blobs and Droplets
  • While Nsp1 is manipulating ribosomes, other viral proteins are busy making new viruses. A half-dozen different proteins come together to make new copies of the virus’s RNA. But something remarkable happens along the way: Together, the proteins and RNA spontaneously turn into a droplet, akin to a blob in a lava lamp.
  • Physicists have long known that molecules in a liquid spontaneously form droplets if the conditions are right. “This is just making salad dressing,” said Amy Gladfelter, a cell biologist at the University of North Carolina.
  • But only in recent years have biologists discovered that our cells regularly make droplets for their own purposes. They can bring together certain molecules in high concentrations to carry out special reactions, shutting out other molecules that can’t enter the droplets.
  • Richard Young, a biologist at the Whitehead Institute, and his colleagues have mixed together SARS-CoV-2 proteins that build new RNA along with RNA molecules. When the molecules assemble, they spontaneously form droplets. The virus likely gets the same benefits as the cell does from this strategy.
  • Given the sophistication of the coronavirus in so many other regards, Dr. Young wasn’t surprised by his discovery. “Why wouldn’t viruses exploit a property of matter?” he said.
Pores and Tunnels
  • Coronaviruses can coax human cells to form new chambers to house their genetic material. But when Montserrat Bárcena, a microscopist at the Leiden University Medical Center in the Netherlands, inspected those chambers, she was baffled: There seemed to be no holes in the membranes, allowing no path for the RNA to get in or out.
  • Recently, Dr. Bárcena and her colleagues took a closer look and discovered a way through. One of the coronavirus’s proteins, called Nsp3, folds into a tunnel, which then plugs itself into the membranes.
  • “It’s a coronavirus escape route,” Dr. Bárcena said. “We had this riddle, and now we have an answer.”
Assembling New Viruses
  • In a matter of hours, an infected cell can make thousands of new virus genomes. The cell’s ribosomes read their genes, spewing out even more viral proteins. Eventually, some of those proteins and the new genomes assemble themselves to make new viruses.
  • This is no easy task, because the coronavirus’s strand of genes is a hundred times longer than the virus itself.
  • Recent experiments suggest that, once again, SARS-CoV-2 uses lava-lamp physics to its advantage. Proteins called nucleocapsids glue themselves to spots along the length of the RNA strand. Together, the molecules quickly collapse into droplets.
  • Dr. Gladfelter speculated that this strategy prevented two strands of genes from becoming tangled with each other. As a result, each new virus winds up with just one set of genes.
  • These droplets are swallowed up inside viral membranes and spike proteins, and the new viruses are ready to escape the cell. To simulate these viruses down to every atom, Dr. Amaro is gathering the emerging pictures of SARS-CoV-2 proteins and RNA. She and her colleagues then construct virtual viruses on supercomputers, each consisting of a half-billion atoms. These machines can then use the laws of physics to simulate the dancing of the viruses every femtosecond: in other words, a millionth of a billionth of a second.
  • Dr. Amaro and her colleagues hope to use her simulated viruses to tackle one of the most contentious questions about C19: how the virus spreads from person to person.
  • When infected people exhale, talk or cough, they release tiny drops of water laden with viruses. It’s not clear how long SARS-CoV-2 can survive in these drops. Dr. Amaro is planning to build these drops, down to their individual water molecules, on her computer. Then she’ll add viruses and watch what happens to them.
  • “I’m pretty confident that probably within a year, we would be able to have the whole virus, including all the bits on the inside,” she said.
Drugs and Vaccines
  • Already, however, the new pictures of SARS-CoV-2 have become essential for the fight against the pandemic. Vaccine developers study the virus’s structure to ensure that the antibodies made by vaccines grip tightly to the virus. Drug developers are concocting molecules that disrupt the virus by slipping into nooks and crannies of proteins and jamming their machinery.
  • The virus’s genome may offer other targets. Drugs may be able to lock onto loops and tangles to prevent the virus from controlling our ribosomes. “It’s very important that you know what the shape is, so you can develop the right chemistry to bind to that shape,” Dr. Rouskin said.
  • Dr. Gladfelter, meanwhile, wants to see if the physics of viral droplets may offer a new line of attack against SARS-CoV-2.
  • “You could get a compound that would make them stickier, make them more jelly,” she said. “There are probably a lot of Achilles’ heels.”
Future Research
  • While the past few months have delivered a flood of data about the virus, some studies have made it clear that it will take years to make sense of SARS-CoV-2.
  • Noam Stern-Ginossar and her colleagues at the Weizmann Institute in Israel, for example, have found evidence that the virus makes proteins that scientists have yet to find.
  • Dr. Stern-Ginossar and her colleagues surveyed the RNA of the virus in infected cells, tallying up all the ribosomes that were reading it. Some ribosomes clustered along known genes. But others were reading genes that had never been found before.
  • Ribosomes sometimes read just a section of the spike protein gene, for example. Presumably they make a mini-spike, which may very well carry out some essential job for the virus. A drug that disables it might cure C19.
  • But scientists can’t even begin to guess at these possibilities, because no one has yet spotted the mini-spike in the wild. And the same will be true for the other new genes, Dr. Stern-Ginossar’s team has found.
  • “Each one will require additional work to figure out what they’re doing,” she said. “Biology takes time.”

Source: The Coronavirus Unveiled: Microscopic Images of SARS-CoV-2

6. C19 can survive up to 28 days on surfaces  

  • Australian scientists have found that the coronavirus (Sars-CoV-2) can survive for up to 28 days on surfaces such as the glass on mobile phones, stainless steel, vinyl and paper banknotes.
  • The national science agency, the CSIRO, said the research undertaken at the Australian Centre for Disease Preparedness (ACDP) in Geelong also found that the coronavirus (Sars-CoV-2) survived longer at lower temperatures.
  • It said in a statement the virus survived longer on paper banknotes than on plastic banknotes and lasted longer on smooth surfaces rather than porous surfaces such as cotton.
  • The research, published in the Virology Journal, also found the virus lasted 10 days longer than influenza on some surfaces.
  • Dr Larry Marshall, the chief executive of the CSIRO, said establishing how long the virus survived on surfaces enabled scientists to more accurately predict and prevent its spread, and so protect the community from infection.
  • The deputy director of ACDP, Dr Debbie Eagles, said the results reinforced the need for good practices such as regular hand washing and cleaning surfaces.
  • “At 20C (68F), which is about room temperature, we found that the virus was extremely robust, surviving for 28 days on smooth surfaces such as glass found on mobile phone screens.”
  • Similar experiments for Influenza A found it survived on surfaces for 17 days.
  • Further experiments were carried out at 30C (86F) and 40C (104F), with survival times for the Sars-CoV-2 virus decreasing as the temperature increased.
  • “While the precise role of surface transmission, the degree of surface contact and the amount of virus required for infection is yet to be determined, establishing how long this virus remains viable on surfaces is critical for developing risk-mitigation strategies in high-contact areas,” Eagles said.
  • ACDP director, Professor Trevor Drew, said the research may help explain the apparent persistence and spread of Sars-CoV-2 in cool environments such as meat processing facilities and how that might be better addressed.

Source: Virus that causes Covid-19 can survive up to 28 days on surfaces, scientists find 

D. Vaccines & Testing

1. More than 30,000 Sign Up To Be Infected With C19 To Test Experimental Vaccine 

  • People around the world are trying their hardest to keep from being exposed to C19, but tens of thousands are hoping to do just the opposite.
  • The volunteers have signed up for “C19 human challenge trials,” in which they would receive an experimental vaccine and then be directly infected with the virus to test the vaccine’s effectiveness.
  • “Human challenge trials deliberately expose participants to infection, in order to study diseases and test vaccines or treatments. They have been used for influenza, malaria, typhoid, dengue fever, and cholera,” said a British group called 1 Day Sooner. “Researchers are exploring whether human challenge trials could support the development of vaccines and treatments for C19.”
  • But the trial has no start date. On their website, the group writes: “Sign up here if you may wish to participate in a human challenge trial for C19 if one were to occur, and, potentially, advocate for the safe and rapid developments of vaccines and treatments.”
  • Still, more than 38,000 people, reportedly from 166 countries, have signed up.
  • In a petition, the group calls on the British government to “ringfence funds to create a Challenge Study Center with sufficient biocontainment capacity to quarantine 100-200 volunteers in C19 human challenge trials.”
  • We need multiple vaccines to meet global demand, and some epidemiologists are considering C19 human challenge trials to quickly narrow the field of promising vaccine candidates. Over 1,400 Britons have already volunteered. In the past, the government has provided funding for clinical trial centers during times of need. Today, the government should embrace the altruism of British volunteers and cement the UK’s leadership in future medical research by doing the same.
  • Among those who have signed up is Estefania Hidalgo, 32, a British photography student who works at a gas station, CNN reported.
  • “I do night shifts there, and it can be very lonely,” Hidalgo told CNN. “No one should be left behind. Old people, poor people, people of color. Everyone just deserves to be healthy.”
  • “This was a way for me to take back control of the situation, to feel like I was in a less hopeless place, and a less hopeless world, and be like, OK, I can do this. To make it better, I chose not to be in fear,” Hidalgo added.
  • While volunteers in such challenge trials are usually paid, experts told CNN that it’s important not to “pay an amount that could edge on coercive.” The network also cited critics as saying “challenge trials have limited use because the young, healthy people who take part don’t represent the broader population.”
  • Yet some experts said such a challenge trial could be useful. “It’s not clear that necessarily the first vaccines to be evaluated are going to be the best vaccines,” Peter Smith of the London School of Hygiene & Tropical Medicine told CNN. “I think there’s a very strong case for exploring challenge trials to evaluate vaccines for a large number of potential Covid vaccines in development.”

Source: GUINEA PIGS: More than 30,000 Sign Up To Be Infected With COVID-19 To Test Experimental Vaccine

2. Positive Preliminary Results for 30 Second Rapid Test  

  • Rapid detection of the coronavirus (SARS-CoV-2), in about 30 seconds following the test, has had successful preliminary results in Mano Misra’s lab at the University of Nevada, Reno. The test uses a nanotube-based electrochemical biosensor, a similar technology that Misra has used in the past for detecting tuberculosis and colorectal cancer as well as detection of biomarkers for food safety.
  • Professor Misra, in the University’s College of Engineering Chemical and Materials Department, has been working on nano-sensors for 10 years. He has expertise in detecting a specific biomarker in tuberculosis patients’ breath using a metal functionalized nano sensor.
  • “I thought that similar technology can be used to detect the SARS-CoV-2 virus, which is a folded protein,” Misra said. “This is Point of Care testing to assess the exposure to C19. We do not need a laboratory setting or trained health care workers to administer the test. Electrochemical biosensors are advantageous for sensing purposes as they are sensitive, accurate and simple.”
  • The test does not require a blood sample, it is run using a nasal swab or even exhaled breath, which has biomarkers of C19. Misra and his team have successfully demonstrated a simple, inexpensive, rapid and non-invasive diagnostic platform that has the potential to effectively detect the SARS-CoV-2 virus.
  • “Our role on this project is to provide viral material to be used for detection by the nanomaterial sensor developed by Mano,” Verma said. “Mano contacted me back in April or May and asked whether we can collaborate to develop a test to detect SARS-CoV-2 infection by analyzing patients’ breath. That’s where we came in, to provide biological material and started with providing the surface protein of the virus, which can be used for detecting the presence of the virus.”
  • Verma, an expert on SARS-CoV-2, synthesized and prepared the antigenic protein of C19 virus in his laboratory, SARS-CoV-2 receptor binding domain protein, for the preliminary testing and determining the sensitivity of our nano sensor. Synthesizing and purification of viral proteins is usual and routine work in a virology laboratory.
  • “Our lab is a virology laboratory, which works on different viruses, and we have been working on SARS-CoV-2 from the beginning of the outbreak,” he said. “Our genomics and diagnostic group have been sequencing the SARS-CoV-2 from the nasal swabs of C19 patients of the state of Nevada to determine mutational changes in the virus while SARS-CoV-2 circulates in our population.”
  • The team developed co-metal functionalized nanotubes as a sensing material for electrochemical detection of the protein. They confirmed the biosensor’s potential for clinical application by directly analyzing the RBD of the Spike glycoprotein on the sensor.
  • The team plans to move to the next step of sensor validation on the actual C19 patients swabs stored in the Viral Transport Medium and have applied for funding to develop a specific and inexpensive point-of-care sensor for a rapid detection of C19 virus in saliva or breath of infected individuals.
  • The developed approach also has the potential for diagnosis of other respiratory viral diseases by identifying appropriate metallic elements to functionalize nanotubes.

Source: COVID-19 rapid test has successful lab results, research moves to next stages

3. Abbott’s coronavirus antibody test gets FDA’s emergency use approval  

  • Abbott Laboratories said Monday it was granted emergency use approval by the Food and Drug Administration (FDA) for a coronavirus antibody test that can signal a recent or prior infection of C19.
  • The AdviseDX test, which detects the Immunoglobulin M (IgM) antibody in a blood sample, differs from another Abbott test which looks for the IgG antibody.
  • The IgM antibody is used to determine whether someone had a recent C19 infection, as it becomes undetectable after several weeks, whereas an IgG antibody remains detectable in the body for a longer period of time.
  • “Abbott has developed tests to detect the virus at each stage of infection so doctors and their patients are equipped with knowledge of how they are responding to the virus and progressing through recovery,” Robert B. Ford, the company’s president and chief executive officer, said in a press release Monday. “Antibody tests will continue to play an important role to better understand the virus, the prevalence of C19 in an area and where a patient may be in their recovery.”
  • The company said the AdviseDx test has demonstrated a 99.56% specificity and 95% sensitivity for patients tested 15 days after symptoms began.
  • Abbott has had seven other tests receive emergency use authorization during the coronavirus pandemic, according to Reuters, which allows for the use of unapproved medical products in an emergency to diagnose, treat or prevent serious or life-threatening diseases with no adequate or approved alternatives. 

Source: Abbott’s coronavirus antibody test gets FDA’s emergency use approval

E. Improved & Potential Treatments

1. Anti-ageing drugs could make C19 vaccines more effective in older people  

  • Unlike fine wine, the human body does not improve with age. Hearing fades, skin sags, joints give out. Even the body’s immune system loses some of its vigour.
  • This phenomenon, known as immunosenescence, might explain why older age groups are so hard-hit by C19. And there is another troubling implication: vaccines, which incite the immune system to fight off invaders, often perform poorly in older people. The best strategy for quelling the pandemic might fail in exactly the group that needs it most.
  • Scientists have known for decades that ageing immune systems can leave the body prone to infection and weaken their response to vaccines. In June, the US Food and Drug Administration announced that a C19 vaccine would have to protect at least half the vaccinated individuals to be considered effective, but protection in older adults might not even meet that bar. “No vaccine is going to be as effective in the elderly as it is in young people,” says Matt Kaeberlein, a gerontologist at the University of Washington in Seattle. “That’s an almost certainty.”
  • The human immune system is mind-bendingly complex, and ageing affects nearly every component. Some types of immune cells become depleted: for example, older adults have fewer naive T cells that respond to new invaders, and fewer B cells, which produce antibodies that latch on to invading pathogens and target them for destruction. Older people also tend to experience chronic, low-grade inflammation, a phenomenon known as inflammageing (see ‘Depleted defences’). Although some inflammation is a key part of a healthy immune response, this constant buzz of internal activation makes the immune system less responsive to external insults. “This overarching, chronic inflammatory state is what’s driving much of the immune dysfunction that we see,” says Kaeberlein. The upshot is a poorer reaction to infections and a dulled response to vaccines, which work by priming the immune system to fight off a pathogen without actually causing disease.
Depleted defences. Graphic showing difference between young and old immune systems.
  • With about 50 C19 vaccine candidates currently being tested in humans, researchers say it’s not yet clear how they will fare in older adults. In its phase I study of 40 people aged 56 and over, Moderna in Cambridge, Massachusetts, reported that its candidate mRNA-1273 elicited similar antibody levels as those elicited in a younger age group. The Chinese biotech Sinovac in Beijing, which trialled its CoronaVac candidate in a phase I/II study that included 421 adults between 60 and 89 years of age, announced in a press release on 9 September that it seems to work as well in older adults as it does in younger ones. However, a phase I study by international pharma company Pfizer and BioNTech in Mainz, Germany, showed that their vaccine BNT162b2 provokes an immune response that is about half as strong in older adults as it is in younger ones. The older adults still produced more antibodies in response to the vaccine than people of a similar age who had had C19, but it’s not known how these levels translate into protection from the virus.
  • Most C19 vaccine trials include at least some older adults. But a recent analysis of 18 such trials found that the risk of exclusion is high. More than half had age cut-offs and many were at risk of excluding older participants for other reasons, including underlying conditions.
  • If C19 vaccines perform less well in older adults, researchers might be able to find ways to tweak the shot itself to elicit a stronger response. Some influenza vaccines, for instance, include immune-boosting ingredients or higher doses of the viral antigen. But some scientists say there is a better option. They are developing and testing drugs that could improve how older adults respond to vaccines and might also help them fight viruses more effectively in the first place. Rather than working with the limitations of the ageing immune system, they are planning to rejuvenate it.
Forever young
  • Many researchers have grown old trying to pinpoint ways to reverse the ageing process. In the past decade, however, they have made serious progress in identifying particular molecular targets that might help in this quest.
  • One promising class of anti-ageing drug acts on pathways involved in cell growth. These drugs inhibit a protein known as mTOR. In the laboratory, inhibiting mTOR lengthens lifespan in animals from fruit flies to mice. “mTOR is one of probably multiple biologic mechanisms that contribute to why we age and why our organ systems start to decline,” says Joan Mannick, co-founder and chief medical officer of resTORbio, a biotech company based in Boston, Massachusetts, that aims to develop anti-ageing therapies.
  • In a study published in 2018 and carried out when Mannick was at the Novartis Research Institutes in Cambridge, Massachusetts, she and her colleagues tried damping down mTOR in elderly adults to see if this could improve immune function and lower infection rate. The 264 participants received a low-dose mTOR inhibitor or a placebo for six weeks. Those who received the drug had fewer infections in the year after the study and an improved response to the flu vaccine. On the basis of her work on mTOR inhibition, Mannick, by then at resTORbio, launched a phase III trial in 2019 to see if a similar mTOR inhibitor called RTB101 could stave off respiratory illnesses in older adults.
  • That trial failed to show the desired effect, perhaps because infections were monitored by self-report of symptoms rather than requiring a lab test to confirm infection, as in the earlier trial. That created “a lot more noise”, says Ilaria Bellantuono, co-director of the Healthy Lifespan Institute at the University of Sheffield, UK, who was not involved in the trial. “A much bigger group would have been required to see a difference.”
  • Still, the data from this and an earlier trial suggested that participants who received the mTOR inhibitor had fewer severe infections from circulating coronaviruses and recovered faster from them than the placebo group. The trials pre-date the emergence of SARS-CoV-2, but they suggest that RTB101 could lessen the severity of infection. resTORbio is now testing that idea in 550 nursing-home residents aged 65 and over.
  • RTB101 is similar to an already approved mTOR inhibitor, the immune-suppressing drug rapamycin. At least four other groups are testing rapamycin in small numbers of infected individuals as a possible C19 therapy; one group is trialling the drug exclusively in adults aged 60 or older.
  • The type 2 diabetes drug metformin also dampens down mTOR’s activity, albeit indirectly. Some studies suggest that people who take metformin are less likely to be hospitalized or die if they contract C19. A small retrospective study in China found that the mortality among hospitalized individuals with C19 taking metformin was 2.9% compared with 12.3% in people who didn’t take the drug. Researchers at the University of Minnesota in Minneapolis analysed data on hospitalized individuals with C19 who had an average age of 75, some of whom were already taking metformin for obesity or diabetes. They found a significant reduction in mortality among women taking metformin, but not among men.
  • Carolyn Bramante, an obesity researcher who led the University of Minnesota study, points out that diseases such as diabetes and obesity lead to some of the same immune deficits as occur in older age. She and her colleagues plan to launch a trial of 1,500 people aged 30 and over to determine whether metformin could help stave off SARS-CoV-2 infection or prevent the worst outcomes in people already infected.
  • Meanwhile, Jenna Bartley, who studies ageing at the University of Connecticut in Storrs, is assessing whether metformin can boost responses to the flu vaccine in a small trial of older adults. The idea, based on her work in mice, is that metformin can improve the energy metabolism of the T cells of the immune system, making them better at detecting new threats. Bartley has finished collecting data, but because her lab was shut down owing to C19, she won’t have the results analysed for a few more weeks.
  • If metformin works against C19, researchers will still have to tease out why. Kaeberlein points out that no one is quite sure how metformin works because it has so many targets. “It’s about the dirtiest of dirty drugs out there,” he says. It was originally used as an anti-influenza drug; Bramante says it helps tamp down inflammation. Aside from the mechanistic unknowns, the advantage is that metformin has been used for decades and is generally safe. Children can take it, as can pregnant women. “Metformin is a medication that you actually could give prophylactically for 12 months without having to do any follow-up,” Bramante says, “and it costs less than US$4 a month.”
Soothing balm
  • mTOR is a classic anti-ageing target, but it’s far from the only one. In fact, many anti-ageing pathways seem to be linked, says James Kirkland, who studies cellular ageing and disease at the Mayo Clinic in Rochester, Minnesota. “That is, if you target one, you tend to affect all the rest,” he says. Many of the immune changes that come with ageing lead to the same result: inflammation. So researchers are looking at drugs that will calm this symptom.
  • Arne Akbar, an immunologist at University College London, has shown that the anti-inflammatory drug losmapimod, which is being developed as a therapy for muscular dystrophy, might help boost immunity. In a 2018 study, the researchers injected chickenpox virus into the skin of elderly adults. Although these people had already been exposed to chickenpox, their immune response was lacklustre, hampered by excess inflammation. When the team gave the study participants losmapimod, it ratcheted down inflammation by about 70% and improved their immune responses.
  • In June, the company currently developing losmapimod — Fulcrum Therapeutics in Cambridge, Massachusetts — launched a 400-person phase III study to investigate whether the drug could prevent death and respiratory failure in older people hospitalized with C19.
  • Another class of drug, called senolytics, helps to purge the body of cells that have stopped dividing but won’t die. These senescent cells are typically cleared by the immune system, but as the body ages, they begin to accumulate, ramping up inflammation. In August, Kirkland and a team at the Mayo Clinic launched a 70-person trial to test whether a senolytic called fisetin, which is found in strawberries and sold as a health supplement, can curb progression of C19 in adults aged 60 or older. They also plan to test whether fisetin can prevent C19 infection in nursing-home residents.
  • “Senescence is really a key factor in ageing,” says Eric Verdin, president and chief executive of the Buck Institute for Research on Aging in Novato, California, who is not involved in the fisetin research. No senolytics have currently been approved for clinical treatment, however. “This is one area that has been much less studied,” he says.
  • Kaeberlein says it’s likely that most companies will pursue anti-ageing drugs as therapies before they test them as prophylactics. “It’s much easier to get a therapy approved in people who are already sick,” he says. He thinks that mTOR inhibitors hold the most promise. “If I had the power to go back to the beginning of this whole COVID pandemic and try one thing, I’d pick mTOR inhibitors — rapamycin specifically,” he says. According to his back-of-the-envelope calculations, if rapamycin works in the same way in people as it does in mice, it could reduce C19 mortality by 90%.
  • Kirkland says he can envisage giving one of these anti-ageing drugs as a primer before vaccination. “We have to figure out ways to target fundamental ageing mechanisms at around the time that we’re vaccinating people,” he says, “but we have to find ways of doing this that are safe and effective.”
Added ingredients
  • If tweaking the immune system proves too challenging, there might be ways to juice up the vaccine itself. For flu, there are two vaccines aimed specifically at people over 65, which help worn immune systems to stage a response. One, Fluzone High-Dose, contains four times the standard amount of flu virus antigens, and the other, Fluad, relies on an immune-boosting molecule called an adjuvant.
  • A team led by vaccinologist Ofer Levy at Boston Children’s Hospital in Massachusetts is working on a C19 vaccine specifically for older adults, using an in-vitro screening system to identify the best adjuvants. “Vaccines were typically developed as one-size-fits-all,” he says. But a lot of features — age, sex, and even the season — affect vaccine responses, Levy says. The best combinations of adjuvant and vaccine they find will be tested in mice and then in humans.
  • But, in general, developing medications to improve immune function seems like a much smarter strategy than creating vaccines specifically for elderly people, says Claire Chougnet, an immunologist at Cincinnati Children’s Hospital Medical Center in Ohio, who is studying inflammation in aged mice. Vaccine development is costly and time-intensive. “In the case of an emerging virus, when you want a quick response, that makes things even more complicated if you have to do two types of vaccine,” she says. Plus, individual vaccines target specific pathogens, but an immune-boosting medication could be used with any vaccine. “That could work for the flu, that could work for C19. That would work for COVID-25,” she says. The approach is “extremely versatile”.
  • Verdin agrees that supporting the older immune system should be a priority. “I think the net result of all this will be renewed interest in understanding the defect in the immune response in the elderly.” That has implications not only for the coronavirus, but also for a host of other diseases, including other viral infections and even cancer. “C19 has brought to the front something that a lot of people have ignored.”

Source: How anti-ageing drugs could boost COVID vaccines in older people 

2. Lab-Made ‘Miniproteins’ Could Block C19 from Infecting Cells  

Lab-Made 'Miniproteins' Could Block the Coronavirus from Infecting Cells
  • While the world waits for a C19 vaccine, many researchers are focused on developing effective therapeutics that can be rolled out quickly and cheaply. Monoclonal antibodies—a potentially promising laboratory-manufactured therapy modeled on antibodies extracted from the blood of recovering patients—made headlines recently when President Trump received a not-yet-approved antibody cocktail made by the company Regeneron. And pharmaceutical giant Eli Lilly recently announced that its monoclonal antibody reduced the risk of hospitalization in 300 people who had mild or moderate symptoms of C19, in a small clinical trial.
  • But David Baker, a biochemist at the University of Washington’s Institute for Protein Design, and his colleagues think they can produce an even better therapy. They have designed a synthetic peptide—a short string of amino acids, the building blocks of proteins—20 times smaller than a monoclonal antibody that is designed to bind to the infamous “spike” protein on the surface of the the coronavirus (SARS-CoV-2) particle. Doing so would directly block the virus from binding to the ACE-2 receptors on human cells, functioning much like an antibody produced by an infected person’s immune system. Baker and his colleagues described these “miniprotein inhibitors” in September in Science. Although the study only tested these synthetic proteins in the lab, mixing viral particles with monkey cells in vitro, he says that unpublished data show they can protect mice and hamsters from SARS-CoV-2 infection.
  • “We built these [tiny proteins] from scratch based on ‘first principles,’ using computers to model all the biochemical details of a theoretical protein that could stick to the virus,” explains Baker, who was awarded a $3 million Breakthrough Prize earlier in September for his decades of work pioneering the field of synthetic protein design. His team used computers to digitally design more than two million candidate “miniproteins,” crunched the data using algorithms, sifted out 118,000 candidate genes that encode these proteins, manufactured the proteins from scratch, and tested them directly against the virus in the lab—finding that seven designs could effectively bind to and thus disable the virus.
  • Over the course of 3.5 billion years evolution has produced an incredible array of proteins and peptides. In recent years biochemists have tracked down and used some of these to create new drugs, such as Eptifibatide, an antiplatelet drug administered to prevent heart attacks whose active ingredient is extracted from the venom of the southern pygmy rattlesnake. The Protein Data Bank, an online repository of protein sequences and educational tools, contains the amino acid sequences and full 3-D structures for more than 160,000 peptides and proteins—but the natural world contains hundreds of millions of proteins.
  • “It’s very challenging to discover in nature a peptide that does exactly what you want it to do,” explains Gaurav Bhardwaj, also a biochemist at the Institute for Protein Design, but who was not involved in the Science study. He is trying to design a bespoke peptide that would prevent SARS-CoV-2 from replicating within human cells. “Now we can computationally explore the possible design configurations for a peptide in order to perform the exact functions that we want.”
  • Every protein’s function depends on its structure. Interactions between the atoms of the protein’s amino acids cause these chains to self-assemble in less than a second into a complex array of spirals and pleats. As the chain of amino acids grows, these helices and rippled sheets stack on top of and around one another into a dizzyingly complex series of folds, and it is these folds that give proteins their shape and function. Yet figuring out how one amino acid sequence turns into a specific fold has been a torturously difficult task, and it was only in the 1990s—with ever expanding databases of protein information—that scientists could begin to link sequence to form.
  • “We can make up completely new proteins that have never been seen in nature because we now understand the nature of protein folding,” Baker says. “Our ability to use computers to design ‘de novo’ proteins has really only come into its own in the last few years–we might not have been able to apply ourselves to C19 if the pandemic had happened five years ago.”
  • Many organizations, including the Gates Foundation, the Open Philanthropy Foundation, and most recently, the committee of the Breakthrough Prize, have supported this work. Although monoclonal antibodies for SARS-CoV-2 are already in clinical trials, Baker says his miniprotein inhibitors have even greater potential to tackle the pandemic because they are 20 times smaller and thus would be cheaper to produce quickly and consistently.
  • Synthetic peptides show enormous potential to be scaled up at low cost to produce robust, bespoke treatments, says Sarel Fleishman of the Weizmann Institute of Science in Israel, who was not involved in the study. But they are still in uncharted territory, putting them at a disadvantage in the race for a cure, he says. “The major advantage of monoclonal antibody treatments is that they are completely ‘human,’ meaning they are already compatible with our immune systems. So they carry a lot less risk than synthetic proteins,” he says. Crossing regulatory hurdles will be a lot more straightforward with monoclonal antibodies, he says, because regulators will already understand what they are dealing with compared with a new and unproven technology.
  • Although synthetic peptides have enormous potential, we need to be cautious about being overly optimistic, adds biochemist Erik Procko of the University of Illinois, who worked as a postdoctoral researcher in Baker’s team, but was not part of this specific study. “The pharmacokinetics of miniproteins”—the ways the human body can metabolize, absorb and excrete them—“will be a barrier to their usefulness as drugs,” Procko says. “Eli Lily’s antibody drug persists in the body for a month; it will be challenging for a small designed miniprotein to match that stability in the blood.”
  • Baker acknowledges that both Fleishman and Procko are correct: “our miniproteins will have to go through the same scrutiny of clinical trials as monoclonal antibodies,” he says, “though it is worth noting that regulatory bodies like the FDA have vast experience with all sorts of drug and therapeutic modalities.”
  • Both Procko and Baker note that miniproteins will very likely need to be administered directly to the lungs by inhalation. Researchers at the University of California, San Francisco, have designed just such an aerosol formulation. The technology, called “AeroNabs,” would be administered by an inhaler or nasal spray. Roughly three times larger than Baker’s miniproteins, the U.C.S.F. ones are modeled on “nanobody” particles found in the immune systems of animals such as llamas, and function similarly: they bind to SARS-CoV-2’s “spike” protein and prevent it from fusing with the ACE-2 receptor on human cells.
  • “Monoclonal antibodies are unlikely to reach the airway spaces of the lungs when given as an injectable drug,” explains Aashish Manglik of U.C.S.F., part of the team that developed AeroNabs. He and his colleagues described their innovation in the preprint database bioRxiv in August. Only 2 percent of monoclonal antibodies injected into the bloodstream tend to reach the pulmonary spaces, the regions of the lungs through which the virus gains entry in most people—but a drug delivered via aerosol would be able to reach these air sacs, and thus could serve both as a therapeutic and a prophylactic, Manglik says. “We see this as being useful with patients who are in the early stages of infection, or with people at high risk of becoming infected, such as frontline and healthcare workers,” he says. “However, from a technical perspective, what Baker has been able to pull off—designing everything prospectively and not based on an existing structure in nature—is just phenomenal. It’s an exciting time in protein science.”
  • Beat Christen of the Institute of Molecular Systems Biology in Zurich, who was not involved in Baker’s or Manglik’s research, agrees it is an exciting time. “Synthetic biology is progressing very fast in developing vaccines and therapeutics—in a very short time frame we have seen many things pushed to the forefront, and the corporate world is reacting with many spinoffs and startups that have pivoted to this field,” he says.
  • With an increase in corporate interest, however, may come a decrease in public trust—as happened with genetically modified food two decades ago. The technology was largely seen as expensive and unnecessary, driven by corporate profit motives rather than public need. Synthetic peptides—many entirely “unnatural” and “never seen before on earth”—risk falling into the same trap.
  • “But with C19, there is a clear, huge challenge facing humanity,” Christen says, “and if synthetic biology can contribute with new solutions and new therapies, people will easily see the need for it.”

Source: Lab-Made ‘Miniproteins’ Could Block the Coronavirus from Infecting Cells

3. Study to test whether vitamin D can protect people from C19  

  • UK Scientists are looking for volunteers to take part in a trial to see if taking vitamin D can give the immune system a boost against Covid.
  • People who join would be sent pills in the post to take daily for six months if a finger-prick test shows they are deficient in the “sunshine vitamin”.
  • UK residents are already advised to consider taking supplements over winter when vitamin D levels can dip.
  • That is to improve general health, not specifically to stop infections.
Should I take vitamin D?
  • Vitamin D deficiency is more common in older people, in people who are overweight, and in black and Asian people – all of the groups who are at increased risk of becoming very ill with Covid.
  • The trial, led by researchers from Queen Mary University of London and funded by Barts Charity, will use higher doses of vitamin D than regular supplements.
  • Principal investigator David Jolliffe said the trial “has the potential to give a definitive answer” to the question of whether vitamin D offers protection against Covid.
  • “Vitamin D supplements are low in cost, low in risk and widely accessible; if proven effective, they could significantly aid in our global fight against the virus,” he said.
  • Although vitamin D supplements are very safe, taking more than the recommended amount every day can be dangerous in the long run.

Source: Trial to test if Vitamin D protects against Covid 

4. The other race for a virus treatment

  • While many of us are awaiting news of a vaccine, dozens of companies and academic groups are focusing on an alternate defense: monoclonal antibodies. President Trump recently received an infusion of an antibody cocktail made by Regeneron and called it a “cure.”
  • Apoorva Mandavilli, who covers science and global health for The Times, told us that these antibodies — distilled from the blood of patients who have recovered from the coronavirus — were most likely to be effective for treating the elderly or immunocompromised. They also work way faster than vaccines.
  • “If you imagine a situation like a nursing home where they discovered one case, you can give monoclonal antibodies to the other people in that nursing home as a preventative measure,” Apoorva said.
  • A dark horse in the race to develop an antibody treatment is Prometheus, a ragtag group of scientists working in academic labs, the United States Army Medical Research Institute of Infectious Diseases, and an antibody company called Adimab.
  • While Prometheus’s antibody is not expected to be in human trials until late December, it aims to be effective for up to six months. That’s much longer than those made by Regeneron and Eli Lilly that fade in the body within weeks. On Tuesday, news broke that a government-sponsored clinical trial of Eli Lilly’s antibody treatment had been paused because of a “potential safety concern.”
  • With prices that begin at about $15,000 per year, it’s possible that these antibodies will be a realistic treatment option only for rich individuals, even within the United States, and there hasn’t been much discussion about who should have access to the treatment.
  • “There’s been a lot of talk about who will get the vaccine first, how will the government decide the allocation — there has been none of that discussion for monoclonal antibodies,” Apoorva said.

Source: New York Times Coronavirus Briefing

F. Concerns & Unknowns

1. Staggering 86% who tested Covid positive in lockdown had NONE of the official symptoms  

  • A STAGGERING 86% of people who tested positive for the coronavirus during lockdown did not have key symptoms, doctors have warned.
  • The NHS states that a new persistent cough, a high temperature or a loss of taste and smell are the key symptoms to look out for.
  • Researchers at University College London (UCL) have now claimed that a more widespread testing programme is needed to catch cases where symptoms are not always visible or obvious.
  • This they say will help reduce further outbreaks.
  • Experts used data from the Office for National Statistics (ONS) which is based on a large population survey looking at Covid-19 symptoms and Covid test results.
  • The Infection Survey pilot from the ONS included data from 36,061 people living in England, Wales and Northern Ireland.
  • The study, published in Clinical Epidemiology looked specifically at these patients who tested between April 26 and June 27 this year and whether or not they had any symptoms.
  • The experts have now revealed that 115 people (0.32 per cent) had a positive test result.
  • Looking at participants with the top three Covid symptoms highlighted by the NHS and just 158 (0.43 per cent) experienced these on the day they were tested.
  • Of the 115 patients that tested positive, 16 (13.9 per cent) reported symptoms in contrast to 99 (86.1 per cent), who did not report any symptoms on the day they were tested.
  • Experts have previously urged the government to list other symptoms as official warning signs and the study also included data on people who reported symptoms such as fatigue and shortness of breath.
  • Of those who tested positive for the virus, 25 (23,5 per cent) were symptomatic while 88 (76.5 per cent) were asymptomatic on the day of testing.
  • Professor Irene Petersen (UCL Epidemiology & Health Care) said the fact that so many people who tested positive were asymptomatic on the day of testing “calls for a change to future testing strategies”.
  • She continued: “More widespread testing will help to capture “silent” transmission and potentially prevent future outbreaks.
  • “Future testing programmes should involve frequent testing of a wider group of individuals, not just symptomatic cases, especially in high-risk settings or places where many people work or live close together such as meat factories or university halls. In the case of university halls, it may be particularly relevant to test all students before they go home for Christmas.
  • “Pooled testing could be one way to help implement a widespread testing strategy where several tests are pooled together in one analysis to save time and resources on individual testing.
  • “This strategy would be an efficient way to test when the overall prevalence is low as negative pooled samples can quickly show a large group of people are not infectious.”
  • As part of the report, the authors also noted various other studies that show that a low proportion of those testing positive for the virus are asymptomatic.
  • They added that this varies from case to case.
  • They reference a case in Bejing where of 262 confirmed cases admitted to hospitals, just three (5 per cent) were asymptomatic.
  • It also looked at reports from Italy that suggest between 40 to 75 per cent of people were asymptomatic.
  • Other studies conducted in Iceland, found that of 13,000 residents, 43 out of 100 with a positive test were asymptomatic.

Source: 86% who tested Covid positive in lockdown had no official symptoms, docs warn 

2. COVID-related delays to colorectal cancer screening causing 11.9% rise in death rates  

  • New research presented today at UEG Week Virtual 2020 has shown that delays in colorectal cancer (CRC) screening caused by C19 has resulted in significantly increased death rates for the cancer.
  • Researchers at the University of Bologna produced a model to forecast the impact of time delays in CRC screening on CRC mortality caused by C19. The results found that moderate (7-12 months) and large (>12 months) delays in screening caused a 3% and 7% increase in advanced stage CRC respectively.
  • Based on survival rates at 5 years for stage III-IV CRC, the results showed a significant 11.9% increase in deaths when comparing a 0-3 month delay to a >12 month delay.
  • CRC (or bowel cancer) is Europe’s second largest cancer killer and the most common digestive cancer. Annually, there are 375,000 newly diagnosed cases in the EU and it claims the lives of over 170,000 people.
  • Screening aids the early detection of CRC, and since the rollout of screening programs across Europe there has been a steady decline in mortality rates. However, since the start of the pandemic, screening programs have been suspended in many areas across Europe.
  • Led author of the study, Professor Luigi Ricciardiello, comments, “Across the globe, healthcare systems are facing serious difficulties while dealing with C19 and it is imperative that support is given to the public and patients throughout the crisis, including for high-impact diseases such as colorectal cancer. Healthcare authorities need to act urgently on how they reorganize activities during C19, without compromising the diagnosis of other high-impact diseases like this research shows.”
  • Unhealthy lifestyles, such as diets high in processed foods, smoking and heavy alcohol consumption are linked to the development of CRC. Symptoms include persistent rectal bleeding, a change in bowel habits, abdominal pain and unexplained weight loss.
  • “Early-stage diagnosis of colorectal cancer is crucial – it’s far easier to treat and enhances optimal patient outcomes”, adds Professor Ricciardiello. “It is therefore essential that vital diagnosis tools, like screening programs, continue and help to prevent mortality rates from rising even further.”

Source: COVID-related delays to CRC screening causing 11.9% rise in death rates, research reveals

3. C19 can infect your eyes as well as your lungs  

  • C19 is primarily a respiratory infection, but experts have suspected the virus can also infiltrate the eyes. Now, scientists have more direct evidence of it.
  • The findings are based on a patient in China who developed an acute glaucoma attack soon after recovering from C19. Her doctors had to perform surgery to treat the condition, and tests of her eye tissue showed evidence of the coronavirus (SARS-CoV-2).
  • The case offers proof that “SARS-CoV-2 can also infect ocular tissues in addition to the respiratory system,” the doctors reported in the Oct. 8 online edition of the journal JAMA Ophthalmology.
  • “It’s been suspected that the eyes can be a source of both ‘in’ and ‘out'” for the novel coronavirus, said Dr. Aaron Glatt, a spokesman for the Infectious Diseases Society of America.
  • That’s why health care workers protect their eyes with goggles or face shields, he noted.
  • It’s not possible to say whether the patient in this case contracted SARS-CoV-2 via her eyes, according to Glatt. But that is a possibility—whether through viral particles in the air or by touching her eyes with a virus-contaminated hand, he said.
  • Another big unknown is whether any lingering virus in patients’ eye tissue will cause problems.
  • According to Dr. Grace Richter, an ophthalmologist at the University of Southern California’s Roski Eye Institute in Los Angeles, “It’s too early to know what having this virus floating around in the eye means for ocular health.”
  • At this point, Richter said, limited eye problems have been seen with C19: A small number of patients develop conjunctivitis (“pink eye”), where the white part of the eye and inside of the eyelid become swollen, red and itchy.
  • The patient in this case suffered acute angle-closure glaucoma—a serious condition in which pressure in the eyes suddenly rises due to fluid buildup. It requires prompt treatment to relieve the pressure, sometimes with surgery to restore the eye’s normal fluid movement.
  • Richter was doubtful the coronavirus directly caused the eye complication. In general, certain anatomical features of the eye make some people vulnerable to acute angle-closure glaucoma, and it can be triggered by medications, she explained.
  • Richter speculated that since the patient was hospitalized and likely received various drugs, that might have been the cause.
  • That is possible, agreed Dr. Sonal Tuli, a clinical spokeswoman for the American Academy of Ophthalmology and chairwoman of ophthalmology at the University of Florida College of Medicine, in Gainesville.
  • Tuli said the patient’s case is “interesting,” but leaves open a number of questions. One is whether the virus present in the eye tissue is actually infectious.
  • The patient was a 64-year-old woman who was hospitalized for C19 on Jan. 31. Eighteen days later, her symptoms had fully resolved, and throat swabs turned up negative for SARS-CoV-2.
  • About a week later, though, she developed pain and vision loss in one eye, and then in her other eye a few days afterward, according to the report by Dr. Ying Yan and colleagues at the General Hospital of the Central Theater Command in Wuhan, China.
  • The patient landed in the hospital again, where she was diagnosed with acute angle-closure glaucoma and cataract. Medication failed to bring down her eye pressure, so her doctors performed surgery—taking tissue samples in the process.
  • Tests of those samples turned up evidence that SARS-CoV-2 had invaded the eye tissues, Yan’s team reported.
  • While it’s not clear how the virus got into the patient’s eyes, the experts agreed the case underscores the importance of eye protection. For health care providers, that means goggles and face shields; for the average person, it’s regular hand-washing and keeping the hands away from the eyes.
  • “I think people don’t realize how often they touch their eyes,” Tuli said.
  • That advice will reduce the chance of any virus, including cold and flu bugs, from coming into contact with the eyes, she noted.
  • While that may be enough in most cases, people caring for someone with C19 at home may want to be extra cautious, Tuli suggested. Wearing eye protection in addition to a mask is a “good idea,” she said.

Source: New coronavirus can infect your eyes as well as your lungs 

4. If You Have This BMI Your Risk of COVID Death Increases  

  • Since early in the pandemic, health experts have warned that those suffering from severe obesity — a body mass index of over 40 — are at an increased risk of severe coronavirus infection and death. Now, the CDC is claiming that even those who are moderately obese have a greater chance of severe illness.
  • This week the CDC updated their guidance, adding that those with a BMI between 30 and 40 are “at increased risk of severe illness from the virus that causes C19.” They also added that those who are overweight, defined by a BMI between 25 and 30, “might be at an increased risk for severe illness from the virus that causes C19.” Read on, and to ensure your health and the health of others, don’t miss these Sure Signs You’ve Already Had Coronavirus.
  • According to the CDC, over 71 percent of Americans over 20 are overweight, obese, or severely obese, while nearly 40% are considered at least mildly obese.
  • The CDC recommends that those who fall into this category take extra precautions. In addition to following the prevention methods outlined on their website — which include mask wearing, social distancing, practicing hand hygiene, and avoiding crowded indoor spaces — they also suggest continuing to treat the preexisting condition.
  • “Take your prescription medicines for overweight, obesity or severe obesity exactly as prescribed,” they suggest. “Follow your healthcare provider’s recommendations for nutrition and physical activity, while maintaining social distancing precautions. Call your healthcare provider if you have concerns or feel sick.”

Source: If You Have This BMI Your Risk of COVID Death Increases, Says CDC 

5. Hearing Loss is a potential symptom of C19  

  • A 45-year-old British man has lost his hearing in one ear after catching the coronavirus – prompting experts to warn that the deadly bug may cause permanent deafness among some patients, according to reports.
  • The man — whose only underlying medical condition was asthma — was referred to an otolaryngologist when he experienced the hearing loss after being treated for C19 at a hospital, The Sun reported.
  • His condition had deteriorated after spending about a month on a ventilator but improved when treated with remdesivir, steroids and a blood transfusion, according to the news outlet.
  • But the man soon developed tinnitus — or ringing — in his left ear and then lost hearing in it.
  • Specialists found no blockages or inflammation in his ear canals. Tests for rheumatoid arthritis, HIV and the flu also came back negative, The Sun reported.
  • “Despite the considerable literature on C19 and the various symptoms associated with the virus, there is a lack of discussion on the relationship between C19 and hearing,” wrote the authors of a report in BMJ, a peer-reviewed medical journal previously called the British Medical Journal.
  • “Hearing loss and tinnitus are symptoms that have been seen in patients with both C19 and influenza virus, but have not been highlighted,” they wrote, adding that the virus has previously been detected in cells that line the ear.
  • “This is the first reported case of sensorineural hearing loss following C19 infection in the UK,” they wrote.
  • “Given the widespread presence of the virus in the population and the significant morbidity of hearing loss, it is important to investigate this further,” the authors added.
  • “This is especially true given the need to promptly identify and treat the hearing loss and the current difficulty in accessing medical services.”
  • The research was carried out at University College London and the Royal National Throat Nose and Ear Hospital in London.
  • The case comes after experts at the University of Manchester said patients who have recovered from the coronavirus have reported a deterioration in their hearing as well as other conditions such as tinnitus.

Source: Man reportedly loses hearing in one ear after contracting COVID-19 

6. A man caught coronavirus twice—and it was worse the second time  

  • A man in the US caught C19 for a second time in the space of just two months, according to a study published in The Lancet Infectious Diseases. That makes him the fifth person to have officially caught the coronavirus twice, after cases recorded in Hong Kong, Belgium, Ecuador, and the Netherlands (and there will certainly be more cases we don’t know about). However, what’s strange about his case is that he had had a worse bout of illness the second time. His doctors compared the genome of the virus during the two illnesses and found they were too different to have been caused by the same infection. There’s only one other recorded instance where this has happened—the case in Ecuador.
  • The 25-year-old man tested positive for the first time on April 18, after experiencing several weeks of symptoms including sore throat, cough, headache, nausea, and diarrhea. He felt fully recovered by April 27, and tested negative for the virus on both May 9 and 26. But just two days later, on May 28, he developed symptoms again, this time with fever and dizziness too. He tested positive on June 5 and needed to be hospitalized after his lungs were unable to get enough oxygen into his body, causing hypoxia and shortness of breath. He had no underlying health conditions. The man has now recovered.
  • Being infected once does not mean you’re protected from being infected again, even if such cases are still vanishingly rare, with just five identified out of nearly 40 million confirmed cases worldwide. That means people who have had C19 still need to stay vigilant, following the advice on social distancing, wearing face masks, and avoiding crowded, poorly ventilated spaces. This was not altogether unexpected: coronavirus experts warned us that other coronaviruses, such as the common cold, are seasonal. However, there are still many questions that researchers are racing to answer. How much protection does having C19 confer? Is that mainly through antibodies or T cells? How long does protection last? What does it mean for the medical treatments that are being developed, or for vaccines? Will we all require a yearly shot rather than a one-off vaccine, for example? If nothing else, this new case is a reminder of how much about this virus we still don’t know.

Source: A man caught coronavirus twice—and it was worse the second time

G. Projections & Our (Possible) Future

1. More Than Half Of All Americans “Plan To Stockpile Food And Other Essentials” For The Chaotic Months Ahead

  • There was a time when preppers were relentlessly mocked, but nobody is laughing now.
  • Today, most Americans are thinking about stockpiling food, and this massive shift in our national mindset has been sparked by concern about what is going to happen in the months ahead. 
  • Many Americans believe that another wave of the coronavirus pandemic is coming, others believe that our ongoing economic depression will get even deeper, and yet others are convinced that the upcoming election could produce widespread violence.  Of course there have always been people that have been deeply alarmed about future events, but we have never seen anything quite like this. 
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  • In fact, a brand new survey has found that over half of all Americans are currently planning “to stockpile food and other essentials”…
    • Slightly more than half of Americans in a recent poll from Sports and Leisure Research Group say they already have or plan to stockpile food and other essentials. The chief reason: fears of a resurgent pandemic, which could lead to disruptions such as new restrictions on businesses. On Oct. 2, the number of C19 cases in the USA was its highest in almost two months.
  • People still remember the shortages that we witnessed earlier this year when the coronavirus pandemic first erupted in this country, and those that ended up being stuck at home without enough toilet paper would rather not repeat that experience.
  • So as the mainstream media continues to hype a new wave of the pandemic, we should expect to see Americans hitting the grocery stores really hard.  And according to data company Envestnet Yodlee, there is evidence that this is already happening…
    • Already, there’s some evidence that grocery sales are rising, according to data from industry sources. The typical bill for a trip to the grocery store rose to $72 for the week ended October 6, or 11% higher from the week before, according to data company Envestnet Yodlee.
    • “That’s the highest we’ve seen since the first week of June and the second-highest since we started tracking this in January,” said Bill Parsons, group president of data and analytics at Evestnet.
  • Fortunately, many grocery store chains anticipated a spike in demand in advance and started stocking up ahead of time.  The following comes from CNN…
    • Grocery stores across the United States are stocking up on products to avoid shortages during a second wave of coronavirus.
    • Household products — including paper towels and Clorox wipes — have been difficult to find at times during the pandemic, and if grocery stores aren’t stocked up and prepared for second wave this winter, runs on products and shortages could happen again.
  • During a time when other retailers all over the nation are failing at a pace that we have never seen before, many grocery store chains are actually experiencing booming sales.
  • And of course I have been warning that this would eventually happen for a very long time.  During a time of crisis, demand for food and other essentials tends to go up and demand for non-essential items tends to go down.
  • Needless to say, this is something that is not just happening in the United States.  All over the world we have seen demand for food on the rise, and this comes at a time when global food production has become increasingly stressed.
  • As a result, food prices all over the world are starting to escalate quite aggressively…
    • Food prices continue rising during the coronavirus pandemic, jeopardizing food security for tens of millions worldwide.
    • On Thursday, the Food and Agriculture Organization (FAO) of the United Nations said world food prices rose for the fourth consecutive month in September, led by surging prices for cereals and vegetable oils, reported Reuters.
    • FAO’s food price index, which tracks the international prices of the top traded food commodities (cereals, oilseeds, dairy products, meat, and sugar), averaged 97.9 in September versus a downwardly revised 95.9 in August.
  • Sadly, this is just the beginning.  Global food supplies will continue to get even tighter, and global demand for food will just continue to shoot higher.
  • So I would stock up while you still can, because prices will never be lower than they are right now.
  • Of course things could soon get a whole lot worse.
  • According to one recent survey, 56 percent of all Americans expect “an increase in violence as a result of the election”.
  • Isn’t that incredibly sad?
  • So it makes sense that so many Americans are making extra preparations for the months that are ahead, because it definitely appears that they could be quite rocky.

Source: More Than Half Of All Americans “Plan To Stockpile Food And Other Essentials” For The Chaotic Months Ahead

H. Lockdowns

1. Swedish Health Chief Said Country Avoided Lockdown To Prevent “Pandemic Fatigue”  

  • At the start of the C19 pandemic, Sweden chose to go for herd immunity by refusing to impose a hard lockdown, meaning bars, restaurants, gyms, workplaces and schools remained open and vulnerable people were told to shield while mandatory mask rules were avoided.
  • Despite the mainstream media predicting that this would lead to massive fatalities, Sweden has recorded under 6,000 coronavirus deaths and now has the lowest death rate in Europe.
  • The Scandinavian country’s GDP fared better than the rest of Europe and now large segments of the population have developed herd immunity, reducing the impact of any potential “second wave.”
  • Illustrating how the country is already virtually back to normal, a young woman posted a video of herself boarding a train in Stockholm showing minimal social distancing and hardly anyone wearing masks.
  • Now the director general of Sweden’s National Board of Health and Welfare reveals that one of the reasons the Swedish government chose not to impose a harsh lockdown was to prevent its population from development “pandemic fatigue.”
    • “We did not choose the path of a complete lockdown of society, because we had other arguments for a systematic response to a pandemic,” said Olivia Wigzell during the Pandemic 2020: Challenges, Solutions, Consequences conference, which was held in Moscow.
    • “We were very afraid, we feared that people would develop such a pandemic fatigue, that people would get tired of restrictions. But in Sweden, practically everyone followed the recommendations,” she added.
  • Sweden’s health care system was never overwhelmed, even at the height of the pandemic, and the country is now in a better position than any other country on the continent, virtually all of which continue to follow disastrous lockdown policies.

Source: Swedish Health Chief Said Country Avoided Lockdown to Prevent “Pandemic Fatigue”

2. Making Sense of Sweden  

  • If you’ve been following the virus news out of Sweden, this fact may surprise you. Sweden has become notorious for its laissez-faire response. Its leaders refused to impose a lockdown in the spring, insisting that doing so was akin to “using a hammer to kill a fly.” They also actively discouraged mask wearing.
  • Ever since, people in other countries who favor a more lax approach have held up Sweden as a model. Recently, as new cases have surged in other European countries, some of Sweden’s defenders have claimed vindication.
  • How are you supposed to make sense of all this? Several readers have asked me that question, and the answers point to some lessons for fighting the virus. I think there are three key ones from Sweden:
1. It is not a success story 
  • Over all, Sweden’s decision to let many activities continue unabated and its hope that growing immunity to the virus would protect people does not look good. The country has suffered more than five times as many deaths per capita as neighboring Denmark and about 10 times as many as Finland or Norway.
  • “It was a terrible idea to do what they did,” Janet Baseman, an epidemiologist at the University of Washington, told me.
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2. But Sweden did more than some people realize 
  • It closed schools for students ages 16 and older. It encouraged residents to keep their distance from one another. And it imposed the ban on big gatherings, which looks especially smart now.
  • Compared with other viruses, this one seems especially likely to spread in clusters. Many infected people don’t infect a single other person, while “as few as 10 to 20 percent of infected people may be responsible for as much as 80 to 90 percent of transmission,” The Atlantic’s Zeynep Tufekci has explained.
  • Given this, it’s less surprising that Sweden’s recent virus performance looks mediocre rather than horrible.
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3. Swedish officials have been right to worry about “sustainability” 
  • Strict lockdowns bring their own steep costs for society. With a vaccine at least months away, societies probably need to grapple with how to restart activities while minimizing risk.
  • Sweden’s leaders do not seem to have found the ideal strategy, but they are asking a reasonable question. “We see a disease that we’re going to have to handle for a long time,” Anders Tegnell, Sweden’s top epidemiologist, told The Financial Times, “and we need to build up systems for doing that.”
  • The fact that Sweden is no longer an extreme outlier in new virus cases — even as life there looks more normal than in most places — offers a new opportunity to assess risk.

Source: Making Sense of Sweden

I. Johns Hopkins COVID-19 Update

October 14, 2020

1. Cases & Trends

Overview
  • The WHO COVID-19 Dashboard reports 38.00 million cases and 1.08 million deaths as of 10:00am EDT on October 14. 
United States
  • The US CDC reported 7.87 million total cases and 214,446 deaths. The US daily C19 incidence continues to climb, now up to 50,181 new cases per day, the first time above 50,000 daily cases since August 17. At this pace, the US should surpass 8 million cumulative cases in the next 4-5 days. The US C19 mortality continues to hold steady at approximately 675-700 deaths per day. It has been approximately 4 weeks since the US C19 incidence began its current surge. C19 mortality has not yet shown indication of an increase at the national level, but as discussed below, some states are reporting expected increases in C19 mortality, following several weeks of increasing incidence.
  • More than half of all US states have reported more than 100,000 cases, including California with more than 800,000 cases; Texas and Florida with more than 700,000; New York with more than 400,000; Georgia and Illinois with more than 300,000; and Arizona, New Jersey, North Carolina, and Tennessee with more than 200,000. We expect Texas to surpass 800,000 cumulative cases in the next several days.
  • While the national average daily mortality has not yet started to increase, state-level mortality in some parts of the country are beginning to exhibit expected surges, following several weeks of increased incidence. Many state C19 websites or dashboards do not display incidence and mortality data in a way that facilitates this analysis; however, some independent efforts do, such as the STAT News C19 Tracker. While a number of states are beginning to exhibit increasing C19 mortality, several notable examples stand out.
  • Wisconsin’s summer resurgence began in mid-June, and its current surge started in early September. The corresponding increases in mortality started around mid-July and late September, respectively—both lagging the incidence trend by approximately 3 weeks. Wisconsin’s C19 mortality has doubled since the end of September. In Utah, the current surge began in mid-September, with incidence tripling since that time. Approximately 2 weeks later, the mortality began to surge as well, increasing by 400% since then. Missouri’s C19 incidence began increasing in mid-June, peaked in mid-August followed by a slight decrease, and then surged again starting in early September. Missouri’s mortality has followed a similar trend, doubling from mid-July to early September and then doubling again from mid-September to now. North and South Dakota are both exhibiting substantial spikes in mortality. North Dakota’s current surge in incidence began around mid-August, which was followed by a surge in mortality starting in early September. North Dakota’s C19 incidence has tripled since the start of the surge, and its mortality has increased by more than 400%. South Dakota’s surge began in mid-August as well, and the increase in mortality followed approximately 3-4 weeks later. South Dakota’s C19 incidence and mortality have both increased nearly 500% over that time.
  • Notably, North and South Dakota and Utah have relatively small populations, so the total number of daily deaths remains low (ie, fewer than 15 per day). On a per capita basis, however, South Dakota’s daily mortality (0.65 daily deaths per 100k population) is more than double the national average (0.25 deaths/100k), and North Dakota’s (1.44 deaths/100k) is nearly 6 times the national average. The mortality in both states is still increasing rapidly. Utah went from 0.03 daily deaths per 100k population—12% of the current national average—to 0.15 deaths per 100k—up to 60% of the current national average—in less than 3 weeks.
  • A number of other states have exhibited similar trends with respect to incidence and mortality, but not necessarily to the same degree as these examples. 
  • The Johns Hopkins CSSE dashboard reported 7.88 million US cases and 216,278 deaths as of 1:30pm EDT on October 14.

2. ARIZONA SOCIAL DISTANCING & MASK ORDERS 

  • A study conducted by state health officials in Arizona (US) and the US CDC C19 Response Team evaluated the effects of social distancing measures implemented in Arizona. The study, published in the CDC’s MMWR, found that C19 incidence began to stabilize and then decrease approximately 2 weeks after the implementation of a series of social distancing measures that aimed to mitigate community transmission risk. The researchers evaluated trends in the 7-day average of Arizona’s daily C19 incidence from January 22-August 7, compared against the dates that various social distancing measures were implemented at the state and local levels.
  • From June 1 to June 15, approximately 2-4 weeks after the state’s “stay at home” order ended, Arizona’s average daily incidence increased by more than 150%, which prompted state and local governments to take action. On June 17 the state government permitted local jurisdictions to mandate mask use, and a number of county, city, and tribal governments did so over the following week, covering approximately 85% of the state’s population. Additionally, state officials strengthened social distancing restrictions, including limiting the size of large gatherings, closing or limiting operations at “businesses where mask use and social distancing were difficult to maintain” (eg, restaurants, bars, and gyms/fitness centers), and encouraging mask use in areas where local mandates were not in place. In late June/early July, approximately 2 weeks after local mask mandates began to take effect, Arizona’s C19 peaked and then began to decline. Arizona’s daily incidence decreased 75% from its peak, following the sustained use of local and statewide C19 community mitigation measures. While this study is not able to determine a causal relationship between the measures and decreased transmission, the relative timing of the implementation and the decrease in incidence provide further evidence that social and physical distancing and mask use could be key tools in mitigating SARS-CoV-2 transmission risk.

3. NEW YORK CITY 

  • In an effort to contain emerging C19 hotspots, New York City implemented neighborhood-specific control measures. The restrictions are implemented based on hotspot zones, designated as Red, Orange, or Yellow based on the incidence rate (as well as areas not currently designated as hotspots), and the restrictions include limitations on the operation of schools; businesses, including restaurants and bars; places of worship; and large gatherings. During the first weekend of the newly imposed social distancing and mask requirements, New York City issued 62 summons and more than $150,000 in fines to individuals and organizations for violations of the new policies.
  • Notably, the affected areas predominantly affect Orthodox Jewish communities, which have been singled out by state and local officials, including New York Governor Andrew Cuomo and New York City Mayor Bill DeBlasio, for not adhering to social distancing policies, including large gatherings for Jewish holidays. Notably, 5 of the summons issued over the weekend were to places of worship. Some in the community and neighborhoods have protested the new restrictions, arguing that they are facing discrimination while the rest of the city continues to operate under much looser social distancing policies. The protests led to the arrest of one local activist on charges of inciting a riot as well as unlawful imprisonment of a journalist, following an alleged assault of journalist reporting on the protests. Local Catholic leaders have also opposed the new restrictions, which limit the capacity at all places of worship in the affected areas. While the effort aims to avoid blanket, city-wide restrictions by targeting higher-risk areas, it is unclear if the highly localized restrictions could be effective in reducing transmission and preventing spillover of the virus into other parts of the city.

4. HOSPITAL PREPAREDNESS 

  • A study published in Infection Control and Hospital Epidemiology examined the preparedness of US community hospitals, as opposed to large academic medical centers, during the US C19 epidemic. The researchers surveyed 50 community hospitals across 6 states in the Southeast region in April and May to determine the availability of critical personal protective equipment (PPE), including face masks and shields, N95 respirators, and powered-air purifying respirators (PAPRs). The survey also asked about other C19 practices, including patient and staff screening, universal mask use, and suspension of non-essential procedures.
  • Among the respondents, 48% of community hospitals reported an insufficient supply (ie, “almost out or none” or “few days supply”) of PAPRs, 30% with insufficient supply of N95 respirators, 26% with insufficient surgical masks, and 16% with insufficient face shields. Additionally, approximately 80% of these hospitals implemented strategies to extend their supply of PPE, including extending use of various PPE items—including face masks, respirators, and face shields—or disinfecting and reusing them. The survey provides further data that community hospitals have struggled to maintain adequate PPE supply during their response to C19.
  • More than 75% of the hospitals reported implementing universal masking for staff, patients, and visitors, while only 8% mandated mask use for only healthcare providers. The vast majority (90%) implemented some form of daily screening for hospital staff. By the time the survey was conducted, some facilities had begun to resume some non-essential procedures, including elective surgeries, although the degree to which this occurred varied by facility. Finally, approximately 30% of hospitals utilized on-site laboratories for SARS-CoV-2 testing, and nearly 12% utilized local health department laboratories. The report indicates that at least 30% utilized major private laboratory networks (Quest and LabCorp), but it does not specify how the remaining hospitals managed testing demand.

5. EARLY TRANSMISSION DYNAMICS 

  • A study by the US CDC C19 Response Team, published in the US CDC’s MMWR, examined SARS-CoV-2 transmission dynamics among different age groups in US hotspots during the US summer resurgence. This study builds on previous analysis of US hotspot areas. The study included 767 US counties that were identified as C19 hotspots in June and July—defined as reporting more than 100 C19 cases over a 7-day period and increasing incidence over the previous 3-7 days—which represented approximately 24% of all US counties and 63% of the entire US population.
  • The researchers found that test positivity among individuals aged 0-17 and 18-24 years began to increase approximately 1 month before the county qualified as a hotspot. Test positivity increased progressively in older age groups, following a surge among the younger population. On average, test positivity at the time a county was identified as a hotspot was highest among the 18-24 age group (14%), followed by the 0-17 age group (11%). The test positivity decreased with age among older age groups: 25-44 years (10%), 45-64 years (8%), and 65 years and older (6%). The South and the West regions reported higher test positivity across all age groups during this period, which corresponds to the regions that were most severely affected during the summer.
  • The findings support the idea that transmission among younger portions of the population precedes increased risk among older individuals. It is important to reduce transmission of SARS-CoV-2 in younger population groups in order to protect older, more vulnerable portions of the population. 

6. HANDWASHING 

  • A study by the US CDC C19 Response Team, published in the US CDC’s MMWR, aimed to understand how handwashing behavior in the US has changed since the start of the C19 pandemic. The researchers compared survey data from October 2019, prior to the emergence of SARS-CoV-2, to a survey administered in June 2020 to evaluate how public perceptions and behaviors had changed with respect to handwashing. The survey data was collected from Porter Novelli Public Services’ fall and summer ConsumerStyles surveys. The fall survey included 3,624 respondents, and the summer survey included 4,053 respondents. Both surveys asked participants to select from 6 options (as many as applicable) in which they “would be likely to remember to wash their hands”: (1) after using the bathroom at home; (2) after using the bathroom in public; (3) after coughing, sneezing, or blowing one’s nose; (4) before eating at home; (5) before eating at a restaurant; or (6) before preparing food at home.
  • The researchers identified a statistically significant increase in the odds of participating in 4 of the 6 situations, all of them except before preparing food and after using the bathroom in public. Both of these scenarios had high participation in the fall 2019 survey, so there was not much room for improvement for those 2 options. It is important to note that the survey did not ask participants whether their individual behavior had changed—only the scenarios in which they would wash their hands—nor did it ask about C19 in the context of handwashing behavior. These findings do, however, provide evidence that handwashing behaviors have changed since the start of the C19 pandemic.

7. VACCINE CLINICAL TRIALS 

  • Johnson & Johnson (J&J) announced that it has paused the Phase 3 clinical trial for its candidate SARS-CoV-2 vaccine due to an unexplained illness in one of the participants. In a press release this week, J&J did not share detailed information about the adverse event. The company emphasized that the “study pause” is not uncommon in vaccine trials and that it differs from a “regulatory hold,” which would be mandated by a regulatory authority (eg, US FDA). It is still uncertain if the participant who experienced these events was part of the vaccinated group or the placebo group, and more information is expected to be released in the coming weeks.
  • This is the second leading SARS-CoV-2 vaccine candidate to pause a clinical trial in the US. AstraZeneca’s Phase 3 clinical trial has not yet restarted in the US after pausing in September, although trials have resumed in other countries. Additionally, Eli Lilly also suspended an ongoing trial for its monoclonal antibody cocktail this week due to safety concerns. The pauses in these trials reinforce the critical need to conduct large-scale clinical trials to evaluate efficacy and identify adverse events that may occur too infrequently to be captured in smaller study groups. The pauses and relative transparency from these pharmaceutical companies provides some measure of confidence that the trials are being conducted in an ethical manner and that safety remains a high priority. 

8. HERD IMMUNITY 

  • Three professors published an open letter calling for an approach to containing the C19 pandemic that they call “Focused Protection.” The document, titled The Great Barrington Declaration argues that existing social distancing and other community mitigation policies risk long-term public health impact, and the proposal aims to achieve herd immunity in the absence of vaccination. The authors call for those “at minimal risk of death to live their lives normally [while] protecting those who are at highest risk.” In support of this plan, they call for lower-risk individuals to return to normal social activity—including in-person school and extracurricular activities and normal operations at restaurants, bars, and other businesses—and essentially isolating higher-risk individuals.
  • A number of health experts have highlighted the problematic nature of this proposal. Notably, UN Secretary-General Dr. Tedros Adhanom Ghebreyesus described a herd immunity approach in the absence of a vaccine “unethical.” Beyond the expected increase in C19 hospitalizations and deaths that would accompany increased incidence among lower-risk populations, public health experts have highlighted a number of problems with the plan. Evidence continues to emerge about longer-term health effects from C19, including among previously healthy individuals and those who do not experience severe acute illness. Increased incidence, even among lower-risk populations, could also risk patient surge that could threaten health systems, particularly as the Northern Hemisphere approaches influenza season. While documented cases of reinfection have been limited so far in the pandemic, it remains unclear how long immunity conferred by natural infection can last. Additionally, it is clear that transmission among certain populations (eg, correctional facilities, schools) can quickly spread to households and the community, so increasing transmission among lower-risk individuals is likely to increase transmission risk for higher-risk individuals. 

9. SCHOOL SCREENING & TESTING 

  • The Johns Hopkins Center for Health Security collaborated with the Duke University Margolis Center for Health Policy, with support from The Rockefeller Foundation, to develop guidance for implementing SARS-CoV-2 testing protocols at schools. The report outlines a framework for screening and testing at schools to mitigate school-based transmission risk. The framework enables schools to tailor their testing protocols based on local risk assessments in order to ensure that testing strategies meet local needs. The framework addresses multiple types of tests, including diagnostic and antigen tests; multiple testing strategies, including individual and pooled testing; the likelihood and impact of false positive and negative test results; and other mitigation strategies that can affect transmission risk. In further support of this effort, The Rockefeller Foundation is collaborating with the US Department of Health and Human Services to distribute at least 12,000 rapid antigen tests to 5 pilot cities to evaluate the framework.
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