Coronavirus Update 9-22

Weekday Edition

September 22, 2020

Without reliable information, we rely on fear or luck.

“Our baseline forecast now assumes that some economies will achieve herd immunity to COVID-19 in 2022, along with most advanced economies. Other countries are likely to have to wait until 2023 to achieve the same. Until herd immunity has been achieve, economies will remain hostage to the virus – shrinking with each new outbreak and expanding quickly as social distancing eases with the subsequent decline in infection risks.”
Analysis by Deutsche Bank

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. Nationwide Trends

5. 6 Midwest States At ‘Tipping Point’

C. New Scientific Findings & Research

1. Coronavirus Researchers Discover How C19 May Trigger Fatal Levels of Lung Inflammation

2. Bradykinin Storm: Potential Cause of Severe Outcomes

3. Children’s immune response against C19 better than adults leads to different theories for treatment and vaccines (!)

4. Discovery of druggable pocket in the Coronavirus Spike protein could stop virus in its tracks

5. Study suggests dengue may provide some immunity against C19 (!)

6. The Core Lesson of the C19 Heart Debate

7. Nanoparticle coronavirus model may speed drug discovery for C19 (Link Only)

8. No link between influenza vaccine and C19 risk (Link Only)

L. Johns Hopkins COVID-19 Update

Notes:

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A. The Pandemic As Seen Through Headlines

(In no particular order)

House GOP Report Reveals Extent Of China COVID-19 Coverup; Slams WHO Over “Gross Mishandling”
CDC removes guidelines saying COVID-19 can travel beyond six feet
Moderna Could Distribute COVID-19 Vaccine By End Of Year, Phase 3 Trial Nearly Done
AstraZeneca, Under Fire for Vaccine Safety, Releases Trial Blueprints
Not trusting FDA, Black doctors’ group creates panel to vet Covid-19 vaccines
Trump accuses Democrats of criticizing coronavirus vaccine for political purposes
UAE health minister takes country’s first dose of Covid-19 vaccine
64 high-income nations join effort to expand global access to Covid-19 vaccines, but U.S. and China do not
Bill Gates: best case scenario for the end of the epidemic is probably 2022
More restrictions expected in Europe as coronavirus spreads rapidly
Madrid rolls out new COVID-19 lockdown measures amid infections surge
Leaders in Madrid have requested the Spanish army’s help in enforcing new stay-at-home orders enacted amid a spike in cases
Fears of 2nd UK lockdown intensify as Prime Minister Johnson meets with constituent nation leaders
UK Prime Minister introduces $18,000 fines for COVID rule-breakers
Texas governor to let many businesses across the state to reopen to 75% capacity and allow nursing home visits
New Zealand is lifting all outstanding restrictions except in Auckland
More Than 20% of Universities Could Fail Because of the Lockdowns
Northern Ireland tightens social distancing rules for 2^nd time in 2 weeks
Cases in Florida, Arizona slow
California 3^rd State to pass 15,000 deaths; Texas on the cusp of same milestone
India tops 5.5 million cases
Iceland closes bars, karaoke parlors
4 more counties in Wales brace for lockdown
Jakarta Readies More Beds as Virus Overwhelms Health System
China says it finds COVID-19 genetic material on Russian frozen squid
Germany sees cases decline
Belgium cases top 100,000
Russia new cases exceed 6,000 again
Myanmar locks down Yangon
France 7-day average tops 10,000 for first time
Former FDA Commissioner Gottlieb expects another outbreak in US
Ireland locks down Dublin
Germany sees cases decline
Belgium cases top 100,000
Widespread Avoidance of Medical Care Found Due to COVID-19 Concerns
Indian couple run street-side classes for poor students
Motorcycle rally with 125,000 bikers sparks fears of COVID-19 spread
Hollywood unions, studios agree on rules to start production
Another COVID-19 fallout: Fertility treatments and new life on hold
Hedge fund Bridgewater set up tent offices in the woods to beat COVID-19
Stocks plunge on COVID-19 lockdown fears, political tensions
Shocking percentage of parents said they’d still let their kids go to a sleepover
Chicago restaurants may use old train cars, portable greenhouses for winter months
People working from home still feel guilty about taking a lunch break
Airlines are wooing passengers with unlimited flight promotions
CDC: 11,000 may have been exposed to COVID-19 on airplanes
Bleach touted as ‘miracle cure’ for coronavirus being sold on Amazon: report
Woman spread coronavirus to 15 people on international flight
NYC Restaurants Debate Whether To Use New 10% COVID Surcharge
Online-Only Student Who’s Never On-Campus Suspended Indefinitely For Attending Party
Melbourne Police Surround & Arrest 2 Elderly Women Resting On Park Bench For ‘COVID Violation’

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. Green highlights indicate a decrease or no change and yellow highlights indicate an increase.

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

1. Cases & Tests

Worldwide Cases:

Total Cases = 31,476,206
New Cases = 230,853
New Cases (7 day average) = 283,094 (-978) (-0.3%)

Observations:

7 day average declines slightly, but is near record high of 285,489 cases
1,000,000+ cases every 4 days (based on 7 day average)

US Cases & Testing:

Total Cases = 7,046,216
New Cases = 36,372
Percentage of New Global Cases = 15.8%
New Cases (7 day average) = 41,105 (-251) (-0.6%)
Total Number of Tests = 98,909,775
Percentage of positive tests (7 day average) = 6.1%

Observations:

7 day average declines for first time since 9/11

2. Deaths

Worldwide Deaths:

Total Deaths = 969,018
New Deaths = 4,133
New Deaths (7 day average) = 5,200 (-36) (-0.7%)

Observations:

7 day average has been mostly trending lower since 2^nd peak on 8/13
Since 2^nd peak, 7 day average has declined 708, a decrease of 12%

US Deaths:

Total Deaths = 204,506
New Deaths = 388

Percentage of Global New Deaths = 9.4%
New Deaths (7 day average) = 768 (-14) (-1.8%)

Observations:

7 day average has been mostly declining since 2^nd peak on 8/4
Since 2^nd peak, 7 day average has declined 34.8%
US percentage of global new deaths falls below 10%

3. Top 5 States in Cases, Deaths, Hospitalizations & Positivity (9/21)

Observations:

Total new cases, daily deaths, and hospitalizations continue to decline across the US.
GA recorded on 2 deaths on 9/21 (lowest total since 8/4/20)

Source: Worldometer and The Covid Tracking Project

4. Nationwide Trends (9/21)

Observations:

Data per the Covid Tracking Project shows the daily death total was 287 deaths on 9/21. Daily deaths have been below 1,000 for the last 5 days.

Source: Worldometer and The Covid Tracking Project

5. 6 Midwest States At ‘Tipping Point’

With the country’s coronavirus epicenter now hovering over the Midwest, the number of states “at a tipping point” for C19 infections has jumped from one to six in the past week.
Americans who live in 33 states — two-thirds of the country — should not be traveling right now, according to the risk-assessment map run by the Harvard Global Health Institute and Brown School of Public Health. The color-coded map provides a simple way for Americans to assess that risk. Each state has a rating of green, yellow, orange or red, based upon the number of new daily cases of C19 per 100,000 people over a seven-day rolling average. States colored red or orange are over the threshold for allowing non-essential travel, according to the scientists.
Based on the tracker’s latest data, six states — North Dakota, Wisconsin, South Dakota, Arkansas, Missouri and Oklahoma — are now colored red, which means they have 25 or more new positive C19 cases every day per 100,000 people. Those states are “at a tipping point” and should be under stay-at-home orders, according to the Harvard and Brown researchers.
A week ago, only North Dakota was in the red zone. Over the past seven days, the Roughrider State’s average tally of new cases climbed a whopping 49%, from 32.1 to 47.7 new daily cases per 100,000 people.
But the week’s biggest mover was Wisconsin, whose caseload jumped an astonishing 146% — from 16.9 to 41.5 new daily cases per 100,000 people — enough to vault it into second position in the country.
Alarmingly, the average number of new daily cases is rising in most high-risk states: up 28% in South Dakota; up 66% in Arkansas; up 23% in Missouri and Oklahoma; and up 14% in Iowa.

27 states are colored orange on the map, which signifies they have 10 or more new daily positive C19 cases per 100,000 people over a seven-day rolling average. These states are experiencing an “accelerated spread” of C19, with “stay-at-home orders and/or test and trace programs advised,” according to the Harvard and Brown researchers.
States labeled yellow on the map are not in the clear. Yellow means there is between one and nine new cases of C19 each day per 100,000 people, which still signifies community spread.
Only Vermont is in the green zone, which means fewer than one new daily case per 100,000 people. That signifies that the disease is “on track for containment.”

Source: Travel Alert: 6 Midwest States At ‘Tipping Point,’ Per Harvard-Brown Covid-19 Tracker

C. New Scientific Findings & Research

1. Coronavirus Researchers Discover How C19 May Trigger Fatal Levels of Lung Inflammation

Responding to the C19 pandemic caused by the novel coronavirus requires models that can duplicate disease development in humans, identify potential targets and enable drug testing. Specifically, access to primary human lung in vitro model systems is a priority since a variety of respiratory epithelial cells are the proposed targets of viral entry.
Now, a team of infectious disease, pulmonary and regenerative medicine researchers at Boston University, studying human stem cell-derived lung cells called type 2 pneumocytes, infected with coronavirus, have shown that the virus initially suppresses the lung cells’ ability to call in the help of the immune system with interferons to fight off the viral invaders and instead activates an inflammatory pathway called NFkB.
“The infected lung cells pour out inflammatory proteins. In the body of an infected person, those proteins drive up levels of inflammation in the lungs,” explains corresponding author Darrell Kotton, MD, the David C. Seldin Professor of Medicine at BUSM and Director of the BU/BMC Center for Regenerative Medicine (CReM).
According to the researchers, the inflammatory signals initiated by the infected pneumocytes attract an army of immune cells into lung tissue laden with infected and already dead and dying cells.
“Our data confirms that the coronavirus blocks cells from activating one of the anti-viral branches of the immune system early on after infection has set in. The signal the cells would typically send out, a tiny protein called interferon that they exude under threat of disease, are instead delayed for several days, giving the coronavirus plenty of time to spread and kill cells, triggering a buildup of dead cell debris and other inflammation,” added Kotton.
The data is based on experiments the research team performed in the laboratory of co-senior author Elke Mühlberger, PhD, associate professor of microbiology at BUSM and a researcher at BU’s National Emerging Infectious Diseases Laboratories (NEIDL). Kotton and other members of the CReM have developed sophisticated models of human lung tissue–three-dimensional structures of lung cells, called “lung organoids,” grown from human stem cells–which they’ve used at BU and with collaborators elsewhere to study a range of chronic and acute lung diseases.
The research team, led by co-first authors, Jessie Huang, PhD, Kristy Abo, BA, Rhiannon Werder, PhD and Adam Hume, PhD, adapted an experimental model previously used to study the effects of smoking cigarettes to study the coronavirus in lung tissue. Droplets of live coronavirus were then added on top of the lung cells, infecting them from the air the way the virus infects cells lining the inside of the lungs when air containing the virus is breathed into the body.
“This adaptation of human stem cell-derived pneumocytes to air, known as an ‘air-liquid interface’ cell culture was a key advance that allowed us to simulate how coronavirus enters cells deep in the lungs of the most severely affected patients,” said co-senior author Andrew Wilson, MD, associate professor of medicine at BUSM. “Type 2 pneumocytes are also infected and injured in patients with C19, making this a clinically meaningful system to understand how the disease injures patient lungs.”
Wilson and Kotton, are also pulmonary and critical care physicians taking care of patients with C19 pneumonia at Boston Medical Center, while also leading their laboratories to produce the human lung cells that were then transported into the NEIDL. There Hume, a senior research scientist in the Mühlberger’s lab, worked in a BSL-4 suit to perform the infections of the cells that the three collaborating teams then analyzed together through weekly zoom calls.
“These cells are an amazing platform to study coronavirus infection,” adds Mühlberger. “They likely reflect what is going on in the lung cells of C19 patients. If you look at the damage coronavirus inflicts on these cells, you definitely don’t want to get the disease.”
These findings appear online in the journal Cell Stem Cell.

Source: Coronavirus Researchers Discover How COVID-19 May Trigger Fatal Levels of Lung Inflammation

2. Bradykinin Storm

Bradykinin is a peptide commonly found in the human body that is involved in a myriad of biological functions—including lowering blood pressure, contracting smooth muscle in the lungs and gut, assisting kidney diuresis, creating pain sensation, and triggering inflammation—and new analysis suggests that it could potentially account for certain unexplained facets of C19 disease.
Researchers at the Oak Ridge National Laboratory and several US universities found that an enzyme known as DABK accumulates as a result of the coronavirus binding to ACE2 receptors, which then triggers an increase in bradykinin in the body. This increased level of the peptide could explain clotting issues in C19 patients that can cause serious effects such as heart attacks or strokes as well “COVID toes.”
Increased bradykinin could also cause lungs to become more watery or release blood and immune cells to their interior, which could cause respiratory distress and breathing issues in patients. The myriad of functions of bradykinin could also potentially be linked to thyroid and neurological symptoms in C19 patients.
The bradykinin hypothesis could also potentially explain increased disease severity in male C19 patients compared to females, as females typically produce twice as much of a specific protein that protects against certain effects of bradykinin over-accumulation.
Bradykinin could also factor into the effects of vitamin D deficiency and corticosteroids in C19 disease progression and severity.
Scientists are currently pursuing treatment options that may address the role of bradykinin in C19 patients, such as repurposing the drug icatibant and beginning clinical trials for new treatments. Further research is required to better characterize any direct or indirect effects of bradykinin in C19 patients.

Source: Johns Hopkins COVID-19 Update

3. Children’s immune response against C19 better than adults leads to different theories for treatment and vaccines

The first study comparing the immune responses of adults and children with C19 has detected key differences that may contribute to understanding why children usually have milder disease than adults. The findings also have important implications for vaccines and drugs being developed to curb C19. The study was published today in Science Translational Medicine and was conducted by scientists at Albert Einstein College of Medicine, Children’s Hospital at Montefiore (CHAM), and Yale University.
The study involved 60 adult C19 patients and 65 pediatric C19 patients (less than 24 years old) hospitalized at CHAM and Montefiore Health System between March 13 and May 17, 2020; 20 of the pediatric patients had the novel multi-system inflammatory syndrome (MIS-C). The patients’ blood was tested for the presence of several types of immune cells, antibody responses, and the inflammatory proteins, known as cytokines, that immune cells produce.
Children with C19 fared significantly better than adults. Twenty-two adults (37%) required mechanical ventilation compared with only five (8%) of the pediatric patients. In addition, 17 adults (28%) died in the hospital compared with two (3%) of the pediatric patients. No deaths occurred among pediatric patients with MIS-C.
“Our findings suggest that children with C19 do better than adults because their stronger innate immunity protects them against the coronavirus,” said co-senior author Betsy Herold, M.D., chief of infectious diseases and vice chair for research in the department of pediatrics at Einstein and CHAM. Kevan C. Herold, M.D., C.N.H. Long Professor of Immunology and of Medicine at Yale School of Medicine, was the other co-senior author on the study.
People have two types of immunity–innate and adaptive. Innate immunity, in which immune cells respond rapidly to invading pathogens of all kinds, is more robust during childhood. Adaptive immunity, the second type of immune response, is more specific and features antibodies and immune cells that target specific viruses or other microbes.
Compared with adult patients, pediatric C19 patients in the study possessed significantly higher levels of certain cytokines associated with the innate immune response. This suggests that young people’s more robust innate response protects them from developing acute respiratory distress syndrome (ARDS)–the hallmark of severe and often fatal C19 cases.
One cytokine in particular, known as IL-17A, was found at much higher levels in pediatric patients than in adults. “The high levels of IL-17A that we found in pediatric patients may be important in protecting them against progression of their C19,” said Dr. K. Herold.
Both pediatric and adult C19 patients were found to make antibodies against the coronavirus’ spike protein, which the virus uses to latch onto and infect cells. Those spike-protein antibodies include neutralizing antibodies, which block the coronavirus from infecting cells. Counterintuitively, the researchers found that neutralizing antibody levels in adult C19 patients who died or required mechanical ventilation were higher than in those who recovered–and significantly higher than levels detected in pediatric patients.
“These results suggest that the more severe C19 disease seen in adults is not caused by a failure of their adaptive immunity to mount T-cell or antibody responses,” said Dr. K. Herold. “Rather, adult patients respond to coronavirus infection with an over-vigorous adaptive immune response that may promote the inflammation associated with ARDS.”
The findings have important implications for C19 therapies and vaccines.
“Our adult C19 patients who fared poorly had high levels of neutralizing antibodies, suggesting that convalescent plasma–which is rich in neutralizing antibodies–may not help adults who have already developed signs of ARDS,” said Dr. B. Herold. “By contrast, therapies that boost innate immune responses early in the course of the disease may be especially beneficial.”
As for vaccines, Dr. B. Herold notes that most vaccine candidates for protecting against coronavirus infection are aimed at boosting neutralizing-antibody levels. “We may want to consider assessing vaccines that promote immunity in other ways, such as by bolstering the innate immune response,” she said.

Source: Study finds that children’s immune response protects against COVID-19

4. Discovery of druggable pocket in the Coronavirus Spike protein could stop virus in its tracks

A druggable pocket in the coronavirus spike protein that could be used to stop the virus from infecting human cells has been discovered by an international team of scientists led by the University of Bristol. The researchers say their findings, published in the journal Science, are a potential ‘game changer’ in defeating the current pandemic and add that small molecule anti-viral drugs developed to target the pocket they discovered could help eliminate C19.
Coronavirus is decorated by multiple copies of a glycoprotein, known as the ‘Spike protein’, which plays an essential role in viral infectivity. Spike binds to the human cell surface, allowing the virus to penetrate the cells and start replicating, causing widespread damage.
In this ground-breaking study, the team headed by Professor Christiane Schaffitzel from Bristol’s School of Biochemistry and Professor Imre Berger from the Max Planck-Bristol Centre for Minimal Biology, used a powerful imaging technique, electron cryo-microscopy (cryo-EM), to analyse Coronavirus Spike at near atomic resolution. Enabled by Oracle high-performance cloud computing, a 3D structure of Coronavirus Spike protein was generated allowing the researchers to peer deep inside the Spike identifying its molecular composition.
Unexpectedly, the research team’s analysis revealed the presence of a small molecule, linoleic acid (LA), buried in a tailor-made pocket within the Spike protein. LA is a free fatty acid, which is indispensable for many cellular functions. The human body cannot produce LA. Instead, the body absorbs this essential molecule through diet.
Intriguingly, LA plays a vital role in inflammation and immune modulation, which are both key elements of C19 disease progression. LA is also needed to maintain cell membranes in the lungs so that we can breathe properly.
Professor Berger said: “We were truly puzzled by our discovery, and its implications. So here we have LA, a molecule which is at the centre of those functions that go haywire in C19 patients, with terrible consequences. And the virus that is causing all this chaos, according to our data, grabs and holds on to exactly this molecule – basically disarming much of the body’s defences.”
Professor Schaffitzel explained: “From other diseases we know that tinkering with LA metabolic pathways can trigger systemic inflammation, acute respiratory distress syndrome and pneumonia. These pathologies are all observed in patients suffering from severe C19. A recent study of C19 patients showed markedly reduced LA levels in their sera.”
Professor Berger adds: “Our discovery provides the first direct link between LA, C19 pathological manifestations and the virus itself. The question now is how to turn this new knowledge against the virus itself and defeat the pandemic.”
There is reason for hope. In rhinovirus, a virus causing the common cold, a similar pocket was exploited to develop potent small molecules that bound tightly to the pocket distorting the structure of the rhinovirus, stopping its infectivity. These small molecules were successfully used as anti-viral drugs in human trials and show promise for treating rhinovirus clinically. The Bristol team, based on their data, is optimistic that a similar strategy can now be pursued to develop small molecule anti-viral drugs against coronavirus.
Professor Schaffitzel said: “C19 continues to cause widespread devastation and in the absence of a proven vaccine, it is vital that we also look at other ways to combat the disease. If we look at HIV, after 30 years of research what worked in the end is a cocktail of small molecule anti-viral drugs that keeps the virus at bay. Our discovery of a druggable pocket within the coronavirus spike protein could lead to new anti-viral drugs to shut down and eliminate the virus before it entered human cells, stopping it firmly in its tracks.”
Alison Derbenwick Miller, Vice President, Oracle for Research, added: “Oracle for Research unites researchers and cloud computing to help bring about beneficial change for our planet and its people. Coronavirus and C19 are causing global devastation, and research efforts to find vaccines and treatments cannot move quickly enough. We are so pleased that Oracle’s high-performance cloud infrastructure enabled Professors Berger and Schaffitzel to examine the molecular structures of the coronavirus spike protein and make this powerful and unexpected new discovery that could help curb the pandemic and save lives.”

Source: Discovery of druggable pocket in the SARS-CoV-2 Spike protein could stop virus in its tracks

5. Study suggests dengue may provide some immunity against C19

A new study that analyzed the coronavirus outbreak in Brazil has found a link between the spread of the virus and past outbreaks of dengue fever that suggests exposure to the mosquito-transmitted illness may provide some level of immunity against C19.
The not yet published study led by Miguel Nicolelis, a professor at Duke University, and shared exclusively with Reuters, compared the geographic distribution of coronavirus cases with the spread of dengue in 2019 and 2020.
Places with lower coronavirus infection rates and slower case growth were locations that had suffered intense dengue outbreaks this year or last, Nicolelis found.
“This striking finding raises the intriguing possibility of an immunological cross-reactivity between dengue’s Flavivirus serotypes and coronavirus,” the study said, referring to dengue virus antibodies and the novel coronavirus.
“If proven correct, this hypothesis could mean that dengue infection or immunization with an efficacious and safe dengue vaccine could produce some level of immunological protection” against the coronavirus, it added.
Nicolelis told Reuters the results are particularly interesting because previous studies have shown that people with dengue antibodies in their blood can test falsely positive for C19 antibodies even if they have never been infected by the coronavirus.
“This indicates that there is an immunological interaction between two viruses that nobody could have expected, because the two viruses are from completely different families,” Nicolelis said, adding that further studies are needed to prove the connection.
The study was being published ahead of peer review on the MedRxiv preprint server and will be submitted to a scientific journal.
It highlights a significant correlation between lower incidence, mortality and growth rate of C19 in populations in Brazil where the levels of antibodies to dengue were higher.
Brazil has the world’s third highest total of C19 infections with more than 4.4 million cases – behind only the United States and India.
In states such as Paraná, Santa Catarina, Rio Grande do Sul, Mato Grosso do Sul and Minas Gerais, with a high incidence of dengue last year and early this year, C19 took much longer to reach a level of high community transmission compared to states such as Amapá, Maranhão and Pará that had fewer dengue cases.
The team found a similar relationship between dengue outbreaks and a slower spread of C19 in other parts of Latin America, as well as Asia and islands in the Pacific and Indian Oceans.
Nicolelis said his team came across the dengue discovery by accident, during a study focused on how C19 had spread through Brazil, in which they found that highways played a major role in the distribution of cases across the country.
After identifying certain case-free spots on the map, the team went in search of possible explanations. A breakthrough came when the team compared the spread of dengue with that of the coronavirus.
“It was a shock. It was a total accident,” Nicolelis said. “In science, that happens, you’re shooting at one thing and you hit a target that you never imagined you would hit.”

Source: Study suggests dengue may provide some immunity against COVID-19

6. The Core Lesson of the C19 Heart Debate

Last Monday, when I called the cardiologist Amy Kontorovich in the late morning, she apologized for sounding tired. “I’ve been in my lab infecting heart cells with coronavirus since 6 a.m. this morning,” she said.
That might seem like an odd experiment for a virus that spreads through the air, and primarily infects the lungs and airways. But coronavirus can also damage the heart. That much was clear in the early months of the pandemic, when some C19 patients would be hospitalized with respiratory problems and die from heart failure. “Cardiologists have been thinking about this since March,” said Kontorovich, who is based at Mount Sinai. “Data have been trickling in.”
Autopsies have found traces of the coronavirus’s genetic material in the heart, and actual viral particles within the heart’s muscle cells. Experiments have found that coronavirus can destroy lab-grown versions of those cells. Several studies have now shown that roughly 10 to 30% of hospitalized C19 patients had high levels of troponin—a protein released into the blood when the heart’s muscle cells are damaged. Such patients are more likely to die than others with no signs of heart injury.
This is worrying for people with severe symptoms, but more recently, a few studies suggested that C19 can cause heart inflammation, or myocarditis, even in people who showed mild symptoms, or had recovered. These results were controversial but concerning. Myocarditis is frequently caused by viruses, and resolves on its own in many cases. But it can progress to more severe heart problems, and is one of the leading causes of sudden death in young adults. These studies contributed to decisions by two college football conferences—the Big Ten and the Pac-12—to cancel their fall season. (The Big Ten has since reversed its call, and the Pac-12 is considering doing the same)
These developments have only added to C19’s mystique. News stories and scientific articles have spun a narrative about a bizarre virus that behaves like no other, and a supposedly respiratory illness that should perhaps be reconsidered as a vascular disease. But several cardiologists and virologists I’ve talked with say such claims are overblown. C19 is a severe disease that should be taken seriously, but it’s not all that strange. It seems that way in part because it is new and extremely widespread, and so commands our full attention in the way that most viral illnesses don’t. Hundreds of researchers are studying it. Millions of people have been infected by it. And every study, every news story, and every unusual detail quickens the pulse.
From a virus’s point of view, the heart is both an easy target and a terrible one. It is easy to reach and invade because it collects blood from all over the body and, unlike the brain, has no protective barrier. But infecting the heart also risks killing the host without triggering symptoms that would allow a virus to easily spread—coughing, sneezing, diarrhea, or vomiting. For that reason, viruses that affect only the heart “do not exist,” says Efraín Rivera-Serrano, a virologist at the University of North Carolina at Chapel Hill.
But viruses can incidentally affect the heart. They do so often enough that in the Western world, they are the most common cause of myocarditis. At least 20 known viruses can trigger this condition, including those that cause influenza, Zika, dengue, and measles.
The list also includes the original SARS virus: One Toronto-based study found its genetic material in seven of 20 autopsied hearts. These hearts also had myocarditis. By contrast, autopsied hearts with traces of the new coronavirus typically don’t (with some exceptions). The virus was there, but whether it was actually doing anything is unclear.
But a virus doesn’t need to be in the heart to wreak havoc. It can cause indirect damage by attacking the lungs and starving the heart of oxygen, or by triggering an inflammatory immune response that affects the entire body. Even viruses that primarily affect the gut (like enteroviruses) or the respiratory system (like adenoviruses) can cause myocarditis in this way, when molecules produced at the site of infection travel through the bloodstream and inflame the heart. Coxsackie B, for example, is the most widely studied cause of viral myocarditis, but is primarily a gut virus that spreads through fecal contamination; it can infect the heart, but it does much of its damage via the immune system.
“To say a virus is cardiac or vascular or respiratory simplifies things too much,” says Paul Checchia, a cardiologist at Texas Children’s Hospital. “Anytime a pathogen invades the body, the whole body reacts.” Coronavirus is no exception. The immune system’s response to this coronavirus can be slow to kick off, but then prolonged and severe. These immune overreactions are similar in kind to those triggered by other respiratory viruses, like influenza, but greater in degree. The heart could potentially be caught in this stronger crossfire.
But how often does that happen? In the early months of the pandemic, it seemed clear that the risk of heart injuries was “directly proportional to the severity of the illness,” says Neel Chokshi, a sports cardiologist at the University of Pennsylvania. But in July, a team led by Valentina Puntmann at University Hospital Frankfurt, in Germany, complicated that picture. The researchers showed that 78% of people who had recovered from C19 (including many who had never been hospitalized) still had some kind of heart abnormality that was detectable on MRI scans two months later. About 60% still had signs of myocarditis.
The study was explosive. It spawned a wave of articles and papers about the possibility that C19 could inflict stealthy and prolonged harm upon the hearts of people who aren’t outwardly sick, and reportedly influenced decisions about whether college athletes should be allowed to play. These intense discussions sparked intense criticism. Other scientists slammed the study for several errors, including data that were missing, reported incorrectly, or analyzed with the wrong statistical tests. The Frankfurt team corrected its paper, and says the main conclusions still stand.
“I think the data are good,” says Tiffany Chen of Penn Medicine, who specializes in cardiac imaging and was not involved in the study. “These were relatively healthy, mild cases of C19, and they had a lot of abnormalities. It’s unsettling.” But the clinical implications of these findings—what they mean for C19 patients whose symptoms have abated, but whose MRI scans are abnormal—aren’t yet understood, she says.
Viral myocarditis isn’t always a problem. It’s entirely possible that you have had the condition at some point in your life without ever realizing it. Some people recover but have persistent scarring that weakens their heart and increases the risk of problems years down the line. And in a third group, the inflammation rapidly worsens, leading to faulty heartbeats, heart failure, or even death.
The latter two outcomes are rare, but “it’s really hard to give accurate percentages,” says Chokshi. Doctors typically see cases of viral myocarditis only when they fall into the third group, and severe symptoms warrant MRIs and other diagnostic tests. “We don’t do MRIs on everyone who has the flu, so we don’t know how many have inflammation or what their long-term outcomes are,” says Martha Gulati, the cardiology chief at the University of Arizona. For example, in two small pilot studies, Checchia found signs of heart damage in 40 and 55 percent of children who were hospitalized with RSV—a common respiratory virus. “On discharge, they seemed perfectly fine,” he says. “But we couldn’t get funding to look at them months or years down the line.”
Without that information, it’s hard to know what to make of the Frankfurt C19 study or others like it. Yes, some patients have myocarditis—but what does that mean? How do the numbers compare to other respiratory viruses? Will C19 patients with myocarditis recover fully, or will some have long-term problems? Is this virus doing something strange, or are researchers just studying it more intensely than other viral infections? For now, it’s difficult to say.
The worry is that C19 is doing whatever it’s doing at scale. The original SARS epidemic of 2003 infected only 8,000 people, killed slightly fewer than 800, and was over in three months; its impact on the heart was “lost in the historical bin of the scientific literature,” says Checchia. Coronavirus, by contrast, has infected at least 31 million people and killed at least 960,000. Its effects are thousands of times more obvious than its predecessor’s. Even if it’s no worse than any other viral illness, its sheer scope means that a tiny risk of severe long-term problems would still translate to a lot of failing hearts.
Reassuringly, “there hasn’t been an obvious influx of patients being admitted to the hospital with unexplained myocarditis, despite the huge numbers who have had C19,” says Venkatesh Murthy, a cardiologist at the University of Michigan. “I don’t find it convincing that there is a major amount of serious clinically relevant myocarditis in people who are feeling well.”
Still, he and others say that long-term studies are important. “We’re still early,” says Chen. “I don’t think there’s a defined time point when we’d expect to see heart failure, so we have to follow these patients for months or years down the road.”
That can be unnerving for people who are currently sick. Long-haulers, who are struggling with months of debilitating C19 symptoms, are “responding to the media’s interpretation of these studies and, to put it bluntly, are rightfully freaking out,” said Kontorovich, who is part of a team that provides care for long-haulers. But for now, she sees the myocarditis issue and the long-hauler phenomenon as separate matters.
Some long-haulers have been diagnosed with dysautonomia—a group of disorders that disrupt involuntary bodily functions, including heartbeats (which can become inexplicably fast) and blood pressure (which can suddenly crash). But people who have lingering heart problems after viral myocarditis don’t usually experience the chronic symptoms that long-haulers do, and they typically have measurable changes to their hearts that long-haulers don’t. “There may be a connection, but it hasn’t been proved,” Kontorovich said.
College athletes are also facing immediate decisions. In just the past two months, the 27-year-old basketball player Michael Ojo died from a heart attack during a practice, while the 20-year-old football player Jamain Stephens Jr. died from a blood clot in his heart. Both had previously contracted C19.
In a recent study, a research team at the Ohio State University scanned the hearts of 26 college athletes who tested positive for C19 and had mild or absent symptoms. Four of them—15 percent—had signs of myocarditis. But the Ohio study didn’t examine a control group of similar athletes who didn’t have C19, and even healthy athletes experience changes in their heart as they train, including features that are “similar to what you might see with infections or scarring,” says Gulati, the cardiologist at the University of Arizona.
If athletes come down with clinical myocarditis—that is, with obvious signs of heart problems—they’re taken out of play for at least three months to let the infection run its course and to give the heart a chance to bounce back. The question now is: What to do about the people who have subclinical myocarditis after C19, which presents with no symptoms and can be seen only on a medical scanner? Chokshi, the sports cardiologist, says the risk that these abnormalities will lead to heart failure “is very, very low,” but “the outcome is catastrophic.” The American College of Cardiology published guidance advising that all athletes who test positive for C19 rest for at least two weeks, even if they show no symptoms.
Setting myocarditis aside, it still makes sense to stop players from spreading the virus to one another, especially when so many colleges are facing large outbreaks. “There are plenty of reasons to not play football independent of this issue,” Murthy says. “We already have plenty of evidence to take C19 seriously.”
As pandemics get wider, they feel weirder. Ebola was identified in 1976, but its ability to affect eyes, linger in semen, and afflict survivors with long-term complications wasn’t fully appreciated until it infected 28,000 people in West Africa, from 2014 to 2016. Zika was identified in 1947, but its ability to cause microcephaly—a condition where babies are born with small heads—wasn’t noted until the explosive epidemic of 2015.
When millions of people become infected, rare events become commonplace, and phenomena that might typically have gone unnoticed suddenly become prominent. This creates a deceptive sense that the disease in question is stranger than most, and has uprooted the world because there’s something inherently odd about it.
C19 is different only in that everyone is encountering it for the first time during a pandemic. The world has gone from complete ignorance to an onslaught of detail in a matter of months, and those details can seem jarring. The virus affects the heart. Also, the brain. Odd symptoms. A multisystem inflammatory syndrome in children. Cases of reinfection. Some of these phenomena will be particular to the coronavirus. Others would also show up if any new virus infected millions within months.
This is not to downplay the severity of the pandemic. Some claims about C19’s effect on the heart may be overwrought, but that doesn’t mean the virus is harmless. Conversely, the claims that C19 is equivalent to the flu are clearly wrong, but that doesn’t mean anything goes. The reality lies between this false dichotomy and is still grim, as evidenced by the sheer number of infections, deaths, and lingering disabilities. “It’s hard to find a balance,” says Rivera-Serrano. “It’s not an apocalyptic zombie virus that’s so different from everything else and can suddenly do all these things to the body. But you also don’t want to trivialize what is happening.”
Indeed, by bringing underappreciated aspects of viral infections to light, C19 might help to change our understanding of diseases in general. The long-term consequences of viral myocarditis, for example, are still unclear, because “it can be really hard to identify hundreds of people who have all been exposed to the same virus in a relatively short amount of time,” Murthy says. That’s no longer true. And beyond making studies possible, the pandemic also clarifies that such studies are worthwhile. “We have a mindset that this is a problem we need to work on,” Murthy adds.
The heightened focus on C19 allows hype and sensationalism to flourish, but also shines a spotlight on phenomena that have long been consigned to the shadows. For example, many of the lingering symptoms that long-haulers are facing are similar to known chronic conditions such as dysautonomia and myalgic encephalomyelitis, which can be triggered by other viral infections. These illnesses have been dismissed and trivialized for decades. Few doctors know how to deal with them. Few scientists study them. That might change as thousands of people with similar problems are emerging all at once, and are pushing for recognition and research. In a pandemic, experiences that might once have been dismissed grab attention. Perhaps that tells us they should never have been dismissed at all.

Source: What COVID-19 Does to the Heart

D. Vaccines & Testing

1. Could a Century-Old TB Shot Protect Against C19?

3 years ago, doctors in Greece began recruiting 198 older people for a unique experiment. They injected half of them with a century-old tuberculosis vaccine typically given to newborns in the developing world. They gave the other half a placebo. They wanted to find out if the vaccine, called Bacillus Calmette–Guérin, or BCG, would protect older people—not against TB, but more broadly against viral infections.
Results are now in: During the year after receiving the shot, the BCG group had 80% fewer serious respiratory viral infections than the unvaccinated group. The results were published in Cell at the end of August by doctors at the University of Athens Medical School in Greece, and Radboud University Medical Centre in Nijmegen, Netherlands.
That’s a big deal for a few reasons. People 65 years and older are more likely than any other age group to be hospitalized due to respiratory infections such as influenza, and this study is a preliminary signal that some vaccines could have broad beneficial effects beyond protection from a particular disease. And C19, too, is a respiratory viral illness that disproportionately leads to the hospitalization of older people.
“The chances are increased that BCG would have the same effect on C19 as on other viral respiratory infections like the flu,” says Mihai Netea, the senior author of the study and experimental internal medicine chair at Radboud University. Tests of whether BCG specifically protects against C19 are ongoing; there are now at least 20 randomized clinical trials around the world to see whether it can indeed protect health workers and the elderly.
Many scientists now believe that BCG and some vaccines like it that contain a live, weakened virus may act against non-target diseases. A 2016 review commissioned by the World Health Organization found that BCG and the measles vaccines reduce overall mortality by “more than would be expected through their effects on the diseases they prevent.”
“I think that we have to acknowledge that vaccines have effects much broader than the target disease and the effects can be used,” Netea says.
The research that became the Cell study began in 2017, when Netea’s team recruited patients who were visiting the hospital at the University of Athens Medical School. Most were around 80 years old. They were assigned randomly by computer to either the BCG vaccine or placebo group—the scientists were not aware of the assignments as a nurse injected each patient just before their discharge. This process, called “double-blinding,” is meant to reduce bias. The researchers then rang the patients up every month for a year to check on their health. If a doctor had diagnosed them with an illness, the scientists noted this down.
Netea was nervous about patients having an adverse reaction to the vaccination, itself. In aging patients, there’s always a risk that an immune response can overfire, and BCG has traditionally been given to newborns, not the aged.
Then, C19 hit, and observational studies done by scientists such as Luis Escobar, a disease ecologist at Virginia Tech in Blacksburg, Virginia, hinted that nations where newborns get BCG shots are associated with lower C19 mortality. Netea and his colleagues decided to fast track their analysis. In mid-May, they learned that the vaccinated patients had 80 percent fewer moderate-to-severe respiratory infections.
“That is pretty damn good,” says Kim Mulholland, a vaccinologist at the Murdoch Children’s Research Institute in Melbourne, who was more skeptical of broad beneficial effects of vaccines before this study. “This study left me with the feeling that I should go out and get a BCG vaccine.”
Netea’s clinical trial is the first to show the potential of vaccine non-specific effects in the developed world and in older people. But the idea builds upon ongoing observational research in Guinea Bissau, a tiny West African nation, where Peter Aaby, a Danish anthropologist, and his team have tracked almost 200,000 infants since the 1990s. BCG was first introduced in Guinea Bissau in the late 1980s, and the Danish scientists subsequently saw that children who received the vaccine did better in terms of overall survival than ones who did not. They eventually attributed this to the vaccine protecting the children against a variety of other diseases, although they were not able to elucidate a mechanism by which this might be happening. For example, the results of a study they published in 2005 concluded that BCG may protect children against lung infections caused by the respiratory syncytial virus (RSV). They have since published other papers concluding that the measles and the oral polio vaccines may also be broadly beneficial.
Aaby calls vaccine non-specific effects he has seen “enormous.” “They are actually more important for child mortality than the specific effects,” he says.
But some public health researchers are unconvinced by the Guinea Bissau data. Many of the studies are from a single population in the developing world, and are observational, says Paul Fine, a communicable disease specialist at the London School of Hygiene and Tropical Medicine in London, who is critical of some of Aaby’s research. The scientists observed the effects of vaccination on the overall wellbeing of the child, but these weren’t double-blind randomized clinical trials, which are the gold standard for research. The scientists and the parents both knew whether or not a kid had received a vaccine, and the scientists could not ethically choose to give a kid a placebo for the sake of comparison. Fine says that on the topic of vaccine non-specific effects, Aaby “has pushed it very hard, and sometimes it’s beyond the boundaries of the data.”
Christine Benn, an epidemiologist at the University of Southern Denmark who is married to Aaby and works with him, says the public health community ignored their work because they couldn’t explain what was happening biologically when vaccine use correlates with improved survival. “It is quite incomprehensible to me, because the basis for medicine today is really epidemiological observation, and not always having the immunological or biological mechanism to explain it,” Benn says.
In 2010, Aaby and Benn were prolifically publishing observations from Guinea Bissau when Netea’s lab stumbled into this turf by accident. Netea’s graduate student Johanneke Kleinnijenhuis, then at Radboud University Medical Centre, was running a routine experiment. She had some blood from graduate students who’d gotten BCG shots before heading to TB-endemic countries for coursework, and was testing the cells against the TB bacterium to see if an immune response was triggered. For the sake of comparison, she also tested the cells against the fungus Candida albicans. To her surprise, she found that the cells also had an immune response to the fungus. “Initially we thought, ‘This is a mistake,’” Netea says. “And then we repeated it. And we saw the same thing.”
He felt disbelief because vaccines aren’t supposed to work this way. The US Centers for Disease Control defines a vaccine as a product that generates immunity to a specific disease, and protects a person from that disease. But the grad student’s petri dish suggested the BCG vaccine could react to more than just TB.
This is how the immune system has been thought to work: When a bug enters us, it aims to invade our cells, take control and replicate. Our bodies mount a forceful attack and trigger inflammation, which kills the invaders quickly and non-specifically. This is the “innate” immune response.
If the invaders escape, the “adaptive” immune response kicks in after a few days. Our bodies assemble killer cells that are highly selective, and target the trespassers and the infected cells. After the war ends, the body stores a copy of the killer cells, so the next time there’s an invasion, the adaptive immune system quickly eliminates the threat. So, a person who has been exposed to, say, a weakened tuberculosis bacterium through a BCG vaccine is theoretically protected against TB for life due to this adaptive memory.
The work of scientists like Netea suggests there’s a third kind of immune response—a “trained” innate immune response. He says that a BCG vaccine not only creates an adaptive memory against TB, it also rewires the innate immune system—that first line of defense. Genes that encode the frontline inflammation defenders remain at the ready for some time, so when any infection happens, the innate immune system reacts instantaneously. He thinks that trained immunity may especially repel respiratory viruses, which come face-to-face with immune cells almost immediately upon invading the lungs. The broad antimicrobial effect, Netea speculates, may last a year, if not more.
But research into vaccine non-specific effects—and to figure out both how and if they might work—is still novel scientific turf. And after C19, some 20 scientific teams began testing BCG to see if they can make a connection between the vaccine and protection against the disease. “What is happening is not in textbooks yet,” says Andrew DiNardo, an infectious disease specialist at the Baylor College of Medicine, who is part of a team running a BCG C19 study in the US. The team is giving either BCG or a placebo to 1,800 health workers, and will track whether the vaccinated group is less likely to contract C19 over six months.
“For the last 30 or 40 years, the typical paradigm is you identify a specific vaccine for a specific problem,” he continues. “People are quicker to overlook something that doesn’t fit into the typical paradigm.”
DiNardo calls the Greece study a “fantastic first step,” especially because it shows that people around 80 years old—the most vulnerable age groups for both respiratory infections and C19—can tolerate the inoculation without adverse effects.
But there are caveats, of course. DiNardo says a second trial in a larger pool of patients will show decisively if Netea’s results can be replicated and if the effect is as large as in the original study. Mulholland of MCRI says the BCG vaccine leaves a prominent scar, so clinical participants with some medical expertise might be able to figure out if they’ve received a vaccine or placebo—thereby ruining the double blind. (Netea says in his experience, the majority of patients do not think about it.) Finally, the strain of BCG administered in the vaccine varies among countries, so its effects may differ by population. That’s why the multi-country BCG C19 trials are so important to hammer down effects, DiNardo says.
Netea agrees this is a first step. He and his colleagues have begun the next step—an 8.5 million Euro clinical trial funded by the Danish government in the Netherlands to re-do their study on a larger scale. The scientists began recruiting more than 5,200 older adults last month. They will follow the patients for three months to see if they contract any serious respiratory illness, including C19, and hope to have results in early 2021.
For Netea, the importance of these trials goes beyond C19. If BCG proves broadly useful, similar trials using live, attenuated, existing vaccines could be quickly started when the next pandemic hits. And if they protect, this could buy society valuable time for the production of a new vaccine, Netea says. “This is important because you don’t have to stop the entire economy. You don’t have to have all this collateral damage of the pandemic,” he says.

Source: Could a Century-Old TB Shot Protect Against Other Respiratory Diseases?

E. Improved & Potential Treatments

1. Vitamin D can help reduce coronavirus risk by 54%

Stop waiting for a miracle drug: A Boston University doctor says a sufficient amount of vitamin D can cut the risk of catching coronavirus by 54%.
“People have been looking for the magic drug or waiting for the vaccine and not looking for something this simple,” said Dr. Michael Holick, professor of medicine, physiology and biophysics at Boston University School of Medicine.
Holick and his colleagues studied blood samples from Quest Diagnostics of more than 190,000 Americans from all 50 states and found that those who had deficient levels of vitamin D had 54% higher COVID positivity compared to those with adequate levels of vitamin D in the blood.
The risk of getting coronavirus continued to decline as vitamin D levels increased, the study, published in the Public Library of Science One peer-reviewed journal shows.
“The higher your vitamin D status, lower was your risk,” Holick said.
Many people are vitamin D-deficient because there are only small amounts in food, Holick said. Most vitamin D comes from sun exposure and many are deprived, especially during winter months.
But the sunshine vitamin is easy to find and relatively cheap in drug stores, and taking vitamin D pills comes at no risk. “It’s perfectly safe,” Holick said.
“It’s considered to be, by many, the nutrient of the decade,” Holick said.
C19 positivity is strongly associated with vitamin D levels in the blood, a relationship that stayed the same across different races, sexes and age ranges, the study states.
Vitamin D suppresses excessive cytokine release that can present as a cytokine storm, a common cause of COVID-related morbidity and mortality.
A deficiency in the nutrient alters the immune system, making one more likely to get upper respiratory infections, Holick said.
Throughout the pandemic, people of color have been disproportionately affected by coronavirus, experiencing a higher risk of acquiring it and having serious complications, according to the CDC.
Holick’s study examined the ZIP codes of people of color and found patients from predominantly Black and Hispanic ZIP codes had lower levels of vitamin D and were also more likely to have coronavirus than in patients from predominantly white, non-Hispanic ZIP codes.
The average adult needs around 2,000 units of vitamin D a day, Holick said. He said he’s been taking 6,000 units a day for decades and is in great health.
Several other studies on vitamin D have shown its benefits to the immune system.
Research published with the National Institutes of Health showed people with lower vitamin D levels were more likely to self-report a recent upper respiratory tract infection than those with sufficient levels.

Another study of more than 11,000 participants published in the British Medical Journal found vitamin D supplementation reduced the risk of acute respiratory tract infection among all participants.
“Vitamin D definitely improves your overall immunity to fight infections,” Holick said.

Source: Vitamin D can help reduce coronavirus risk by 54%: Boston University doctor

2. A Drug Used to Treat Deadly Coronavirus Infections in Cats May Be an Effective Treatment Against C19

Researchers at the University of Alberta have shown that a drug used to treat deadly coronavirus infections in cats could potentially be an effective treatment against the coronavirus. The results were published in the journal Nature Communications.
The study, which was aided by scientists at the U.S. Department of Energy’s SLAC National Accelerator Laboratory, paves the way for human clinical trials, which should begin soon, said Joanne Lemieux, a professor of biochemistry at the University of Alberta and the study’s senior author.
“This drug is very likely to work in humans, so we’re encouraged that it will be an effective treatment for C19 patients,” Lemieux said, although the clinical trials will need to run their course before anyone can be sure that the drug, a protease inhibitor called GC376, is both safe and effective for treating C19 in humans.
In cats at least, GC376 works by interfering with a virus’ ability to replicate, thus ending an infection. Derivatives of this drug were first studied following the 2003 outbreak of severe acute respiratory syndrome (SARS), and it was further developed by veterinary researchers who showed it cures fatal feline affliction.
Lemieux and colleagues at the University of Alberta first tested two variants of the feline drug against the coronavirus protein in test tubes and with the live virus in human cell lines, then crystallized the drug variants in conjunction with virus proteins. Working with Silvia Russi, a crystallographer and beamline scientist for the Structural Molecular Biology program at SLAC’s Stanford Synchrotron Radiation Lightsource (SSRL), the researchers determined the orientation of the cat drug as it bound to an active site on a coronavirus protein, revealing how it inhibits viral replication.
“This will allow us to develop even more effective drugs,” Lemieux said, and the team will continue to test modifications of the inhibitor to make it an even better fit inside the virus.
Aina Cohen, a SLAC senior scientist and co-division head of Structural Molecular Biology at SSRL, said she was excited by the drug’s effectiveness and by SSRL’s ability to help out. “Until an effective vaccine can be developed and deployed, drugs like these add to our arsenal of C19 treatments,” she said. “We are thrilled to learn of these important results and look forward to learning the outcome of clinical trials.”

Source: A Drug Used to Treat Deadly Coronavirus Infections in Cats May Be an Effective Treatment Against COVID-19

3. Experimental cancer drug AR-12 could be a promising C19 treatment

A team of scientists led by Paul Dent, Ph.D., at Virginia Commonwealth University Massey Cancer Center has discovered that an experimental cancer drug called AR-12 inhibits the coronavirus from infecting cells and replicating. Their findings were published online today in the journal Biochemical Pharmacology, and steps are now being taken to develop a clinical trial testing the novel oral treatment at VCU Health.
AR-12 has been studied extensively in Dent’s laboratory as both an anti-cancer and anti-viral drug, with prior peer-reviewed publications from Dent and others showing it to be effective against viruses including Zika, mumps, measles, rubella, chikungunya, RSV, CMV, drug resistant HIV and influenza. Recently, collaboration with Jonathan O. Rayner, Ph.D., at the University of South Alabama and Laurence Booth, Ph.D., from Dent’s lab, has demonstrated that AR-12 is highly effective against the coronavirus.
“AR-12 works in a unique way. Unlike any other anti-viral drug, it inhibits cellular chaperones, which are proteins that are required to maintain the right 3D shape of viral proteins. The shape of the virus is critical to its ability to infect and replicate,” said Dent, who is a professor in the VCU Department of Biochemistry and Molecular Biology and the Universal Corporation Chair in Cancer Cell Signaling and a member of the Cancer Cell Signaling research program at Massey.
One of the cellular chaperones inhibited by AR-12 is GRP78, which is essential for the reproduction of all viruses. GRP78 acts as a sort of cellular stress sensor and is required for the life cycle of all mammalian viruses.
Andrew Poklepovic, M.D., medical oncologist, member of the Developmental Therapeutics research program and medical director of the Clinical Trials Office at Massey, is leading efforts to translate these exciting findings into a clinical trial.
“AR-12 is an oral therapy that has been well tolerated in a prior clinical trial, so we know that it is safe and tolerable,” says Poklepovic. “Most C19 drugs are given intravenously, so this would be a unique therapeutic option and potentially suitable for outpatient therapy, similar to the way one would take an antibiotic.”
Poklepovic hopes to begin enrolling patients in early 2021, but several milestones remain. The team must develop the clinical trial protocol, receive approval from the FDA to test AR-12 on C19 patients and manufacture enough of the drug for the trial.
“For help reaching these significant milestones and moving forward with this research at the accelerated pace that we know is needed, we turned to our colleague at Massey, Said Sebti, who has extensive experience in drug development,” says Poklepovic.
Sebti, Ph.D., associate director for basic research and member of the Developmental Therapeutics program at VCU Massey Cancer Center, and professor of pharmacology and toxicology at the VCU School of Medicine, attracted knowledgeable entrepreneurs to form C19 Therapeutics, which recently licensed AR-12 from VCU in order to raise funds in support of drug synthesis and clinical trial sponsorship.
“We are working to submit the required information for FDA approvals, and we are also in discussions with a local pharmaceutical company to manufacture the drug for the trial,” says Sebti. “We are hopeful that AR-12 will emerge as a treatment option for patients suffering from C19, ultimately saving lives and contributing to the global pandemic solution.”
Another observation made in Dent’s research may also shed light into why African Americans have been more affected by severe illness during the C19 pandemic. People of non-European descent, particularly those with African ancestry, make a protein called ATG16L1 T300, while those with primarily European ancestry make a different variant, ATG16L1 A300.
“We compared matched colon cancer cells, with one set making A300 and the other T300, and found that cells making the T300 form made more GRP78 and more of the virus receptor ACE2,” said Dent. “This, of course, does not prove that those with the T300 form are more susceptible to C19, but it provides a biomarker that could be evaluated to help explain why some people get more severe illness than others.”

Source: VCU study shows the experimental drug AR-12 could be a promising COVID-19 treatment

F. Concerns & Unknowns

1. Stillbirth rate rises dramatically during pandemic

A slew of studies from around the world has reported a disturbing trend: since the coronavirus pandemic started, there has been a significant rise in the proportion of pregnancies ending in stillbirths, in which babies die in the womb. Researchers say that in some countries, pregnant women have received less care than they need because of lockdown restrictions and disruptions to health care. As a result, complications that can lead to stillbirths were probably missed, they say.
“What we’ve done is cause an unintended spike in stillbirth while trying to protect [pregnant women] from C19,” says Jane Warland, a specialist in midwifery at the University of South Australia in Adelaide.
The largest study to report a rise in the stillbirth rate, based on data from more than 20,000 women who gave birth in 9 hospitals across Nepal, was published in The Lancet Global Health on 10 August . It reported that stillbirths increased from 14 per 1,000 births before the country went into lockdown to stop the spread of the coronavirus in late March, to 21 per 1,000 births by the end of May — a rise of 50%. The sharpest rise was observed during the first four weeks of the lockdown, under which people were allowed to leave their homes only to buy food and receive essential care.
The study, led by Ashish K.C., a perinatal epidemiologist at Uppsala University, Sweden, and his colleagues, found that although the rate of stillbirths jumped, the overall number was unchanged during the pandemic. This can be explained by the fact that hospital births halved, from an average of 1,261 births each week before lockdown to 651. And a higher proportion of hospital births during lockdown had complications. The researchers don’t know what happened to women who didn’t go to hospital, or to their babies, so they cannot say whether the rate of stillbirths increased across the population.
The increase in the proportion of stillbirths among hospital births was not caused by C19 infections, says K.C.. Rather, it is probably a result of how the pandemic has affected access to routine antenatal care, which might have otherwise picked up complications that can lead to stillbirth, he says. Pregnant women might have been unable to travel to health facilities for lack of public transport; in some cases, antenatal appointments were reportedly cancelled. Others might have avoided hospitals for fear of contracting SARS-CoV-2, the virus that causes C19, or had consultations by phone or Internet. Disruptions brought about by the pandemic have also been linked to a rise in deaths from heart disease and diabetes.
“Nepal has made significant progress in the last 20 years in health outcomes for women and their babies, but the last few months have deaccelerated that progress,” says K.C..

Global trend

Birth data from a large hospital in London showed a similar trend. In July, Asma Khalil, an obstetrician at St George’s, University of London, and her colleagues reported2 a nearly fourfold increase in the incidence of stillbirths at St George’s Hospital, from 2.38 per 1,000 births between October 2019 and the end of January this year, to 9.31 per 1,000 births between February and mid-June.
Khalil calls this the collateral damage of the pandemic. She says that during lockdown, pregnant women might have developed complications that were not diagnosed, and might have hesitated about coming to hospital and therefore been seen by doctors only when a complication was advanced, when less could be done.
Four hospitals in India also reported3 a jump in the stillbirth rate during the country’s lockdown. And as in Nepal, fewer women had their babies in those hospitals. Referrals of women requiring emergency pregnancy care also dropped by two-thirds. This suggests that more births were happening unattended, at home or in small facilities, according to the authors. Scotland — one of a few countries that collates data on stillbirths and infant deaths monthly — has also detected an uptick in the rate of stillbirths in the months of the pandemic.

Disrupted services

In normal times, the World Health Organization recommends that women be seen by medical professionals at least eight times during pregnancy — even if the pregnancy is judged low-risk — to detect and manage problems that might harm the mother, the baby or both. Much of the risk of stillbirth can be averted if women sleep on their side from 28 weeks’ gestation, stop smoking and notify their midwife or doctor if their baby is moving less. The last trimester of pregnancy is particularly important for regular health checks, but women are typically monitored for risk factors such as restricted fetal growth and high blood pressure throughout pregnancy.
When the pandemic hit, professional bodies for maternity health providers recommended that some face-to-face consultations be substituted with remote appointments to protect women from the coronavirus.
But health-care workers can’t take someone’s blood pressure, listen to their baby’s heartbeat or do an ultrasound remotely, says Warland. Because of this, high-risk pregnancies might have been missed, she says, particularly among first-time mothers who are less likely to know what an abnormality feels like. For instance, St George’s Hospital reported a drop in the number of pregnant women presenting with high blood pressure during the UK lockdown. This suggests that “women with hypertension aren’t being managed as they normally would, and undetected hypertension is a risk factor for stillbirth”, says Warland.
The studies are a call to arms to support maternal and newborn health services, especially in low-to middle-income countries, says Caroline Homer, a midwifery researcher at the Burnet Institute in Melbourne, Australia. “This is not the moment to reduce” these services, she says. Homer says that across the Asia-Pacific region, the maternal-health workforce has pivoted to working on the C19 front line, and antenatal care services have reduced face-to-face contact with pregnant women. In some places, services have shut completely, she says.
But Pat O’Brien, the vice-president of the Royal College of Obstetricians and Gynaecologists in London, says the reasons behind this rise in the rate of stillbirths need further exploration.
“We are aware anecdotally of pregnant women presenting late with reduced fetal movements, which can be a sign their baby is unwell, and of women missing antenatal appointments. This may be due to confusion around whether these appointments count as essential travel, fear of attending a hospital or not wanting to burden the NHS,” says O’Brien.
To understand the full effects of the pandemic on pregnancies, future studies will need to use population-level data to assess outcomes in mothers who opted not to go to hospital and gave birth at home or in smaller facilities during the pandemic, says Emily Carter, a public-health researcher at Johns Hopkins University in Baltimore, Maryland. “Sometimes, we’re missing how dire the situation was, even before the pandemic, for certain segments of the population,” says Carter.

Source: Stillbirth rate rises dramatically during pandemic

2. Colds Nearly Vanished Under Lockdown – Now They’re Coming Back

The question may seem odd in the midst of a global pandemic, but among people in places with serious mask-wearing and social-distancing measures, and with the luxury to hunker down, it is forgivable to wonder: Will I ever get sick again? In the southern hemisphere, in places like Australia and South Africa, winter flu season came and went without a trace. The western United States is coughing through clouds of smoke, and people everywhere have endured wet-eyed allergy seasons. But over the past 6 months, people were far less likely to get sick—at least from respiratory viruses that aren’t called SARS-CoV-2.
But in some places, that’s started to change. Data from Australia and across Europe indicate a surge of at least one other ailment that has been lying mostly dormant: the common cold. Colds are caused by many viruses, but the culprits, at this point, are largely rhinoviruses. That isn’t especially surprising. Rhinoviruses are ubiquitous bugs that normally spread this time of year as schools and day care centers reopen, which in many places they have. “This is exactly what we’d expect during a normal back-to-school season,” says Catherine Moore, a virologist at Public Health Wales.
But this year isn’t exactly “normal.” What has surprised public health officials is to see the quick return of non-Covid respiratory viruses with social distancing and mask rules still in place. And this year, their return has presented a unique headache for a simple reason: Early symptoms of colds and C19 are virtually indistinguishable.
That has added a new wrinkle to C19 testing. In Britain, where C19 cases are surging amidst a severe shortage of tests, emergency department officials have taken to Twitter to plead with parents to stop bringing mildly ill children—whose symptoms often turn out to be caused by a rhinovirus—in for testing, often in the hopes that a negative C19 test that will allow them to return to school. “Wheeze-tastic,” strapped pediatricians gripe on Twitter. Even in Australia, where C19 cases are hovering near zero in most of the country, the return of other respiratory ailments has strained supplies and complicated efforts to fully quash coronavirus by testing for the virus widely.
In some ways, the rise of rhinoviruses is a trial run for C19 testing as more respiratory viruses get back into circulation. The reemergence of colds is less concerning than a surge in influenza that could come this winter. In addition to putting pressure on testing supplies, a bad flu season would tax the same ICU beds, personal protective equipment, and respiratory specialists that health officials hope to save for C19. That could force people back into more strenuous lockdown measures to avoid overburdening the health care system. (Reminder, reader: Get your flu shot.)
Cold season, by contrast, usually exacts its toll quietly. Rhinoviruses are rarely dangerous to anyone but the most medically vulnerable. Their damage is mostly economic, coming in the form of sick days, when people are told to sit tight, drink some fluids, and wait the bug out. Tests are rarely necessary outside of hospitals or surveillance programs, when infections are spotted in a respiratory panel test. But those tests are more expensive and are typically only performed by clinicians after more serious ailments, like the flu, have been ruled out.
Symptoms do not completely overlap, Moore says. A runny nose without fever, for example, is more likely to be a cold, while a case involving a high fever is likely not. But that guidance can be hard to put into practice, especially with kids. “It is incredibly challenging, and I don’t blame anybody who has got a child who is coughing or a bit snotty wanting to get a test,” she says. Still, she says, with C19 tests in short supply, the guidance in the United Kingdom is for the mildly ill to lie low. That’s the same message, she notes, that’s often given during severe flu seasons.
The return of colds has been less pronounced so far in the United States, where schools are less likely to have reopened. But there is evidence that infections are rising. Data from the Seattle Flu Study, which tracks a wide range of respiratory illnesses, indicates rhinoviruses were on the upswing beginning in early August, after nearly vanishing in late spring. The early consensus: It’s time to prepare. “This is paramount for all of us,” says Steven Pergam, a professor of infectious disease at the Fred Hutchinson Cancer Center in Seattle. “Testing labs have been so focused on Covid that we’re trying to shift the focus to identifying when other respiratory viruses are in our communities. It’s going to put on a lot more pressure.”
“Covid presents a challenging dilemma because of the range of symptoms,” says Kelly Wroblewski, director of infectious disease at the Association of Public Health Laboratories. “When you see sniffles in a kid, you’re more likely to want to seek a C19 test.” That confusion could put more strain on a precarious supply chain of swabs, reagents, and testing machines. One focus now, Wroblewski says, is to develop panel tests that can distinguish between various respiratory pathogens that can cause more severe disease, including C19, influenza, and respiratory syncytial virus (RSV), a cold-causing virus that typically follows in the wake of rhinovirus season and can lead to more severe disease in very young and old people.
One reason why rhinoviruses leapt back into action at soon as conditions were right is their sheer ubiquity, says Ian Mackay, an associate professor at the University of Queensland in Brisbane, Australia, who spent years studying “rhinos,” as he calls them. Dozens of rhinoviruses may circulate at one time in a community. “They’re always kicking around, because there are so many of them,” he says. And because the viruses have co-evolved with humans over time, they’re well suited to jumping from person to person and living within us, undetected, during lockdown.
That hermetic quality is distinct from certain strains of influenza, which globe-trot along with international travelers. (Closed borders, plus the timing of stringent lockdowns, are thought to be factors that kept the southern hemisphere’s flu season at bay.) Rhinoviruses were ready to come back as soon as school did. “Rhinos love childcare,” Mackay says. That’s in part because children’s immune systems haven’t yet seen many of those rhinovirus varieties, so kids get sick—or at least the sniffles—again and again and again, and they pass the germs along to others.
A question, however, is why the cold viruses appear to be spreading so quickly abroad now in spite of continued mask-wearing and social distancing. Europeans and Australians may be enjoying more of the finer things in life than Americans, but they’re still battling the same pandemic. The differing structures of the virus may play a role. The virus that causes C19 is what’s called an “enveloped” virus, a ball of protein surrounded by a lipid layer. That fatty external structure is easier to destroy with soap and water, and it’s less likely to remain infectious for long on exposed surfaces. That’s one reason health officials now place more emphasis on masks and distancing to help prevent aerosol and droplet spread of coronavirus, and less on disinfecting grocery bags and doorknobs. Rhinoviruses, however, don’t have that envelope, and are thought to be hardier. “Kids will drag their hands through everything and be festy little carriers of the virus,” Mackay says.
Sebastian Johnston, a leading expert on rhinoviruses at Imperial College London, says that while that’s likely the case, he believes aerosols and droplets are probably still the main route for rhinoviruses to get around—same as the coronavirus. That means masks and distancing help curb those viruses too. But the difficulty of getting kids to uniformly abide by those rules, plus children’s susceptibility to passing colds to each other, plus the viability of surfaces as an alternative route of transmission, are all likely coming together to fuel the current outbreaks. Kids are getting these viruses, somehow—just like any other school year—and then bringing them home with them.
This year, that’s coming at a bad time in places like the UK. The return of cold season has coincided with a surge in C19 cases, and just as people are being required to stay home from work and schools if they have any symptoms of illness. Hence the run on emergency room tests from worried parents, despite government officials urging tests to be used sparingly. “The testing system is overwhelmed by demand, and a lot of that demand will be non-Covid respiratory viruses, which are dominated numerically by rhinoviruses,” Johnston says. “Everybody wants to get their kids back to school, and everybody wants to get their employees back to work.”
“The UK seems to have really stumbled,” Mackay says. “They just weren’t prepared for the throughput.” But even in Australia, the arrival of other respiratory viruses has complicated matters, he adds. The country, which has a low number of C19 cases, is taking the opposite approach from the UK. The idea among Australian public health officials is to hunt down every last chain of C19 transmission—embers that could erupt into another true outbreak, like the “second wave” that recently forced the region around Melbourne back into lockdown. That means the government wants to test as widely as possible, even if symptoms are slight. But now rhinoviruses—and increasingly other common viruses, like adenoviruses and RSV—are putting more strain on that system.
Those challenges and more are likely in store for the United States, where the incidence of new C19 cases remains high, and testing resources have been periodically strapped, especially as more schools and businesses reopen. “You’re seeing more opportunities for a savvy pathogen to get transmitted,” Pergam says. “It’s not just rhino. It’s adeno. It’s parainfluenza. It’s RSV. It’s flu. We are thinking that levels will be lower with social distancing and masking, but we don’t yet know for sure.”
Another unknown, he says, is how all those reemerging viruses will intermingle with the coronavirus. Viruses compete and augment each other in ways that are largely mysterious to us—they coexist in our bodies and change how our immune systems react to other pathogens. That competition is thought to be one reason why the fall colds are cut off by winter flus, and then burst back again in the spring. Will the progress of C19 be changed by other viruses? It’s a strange universe of viruses out there, and C19 is about to meet the competition.

Source: Colds Nearly Vanished Under Lockdown. Now They’re Coming Back

G. CDC Reversals

1. In Stunning Reversal, CDC Says It Published New Guidance On Risks Of ‘Airborne’ C19 “In Error”

After publishing guidance warning about the serious risks of “airborne” infection associated with the coronavirus, the CDC just seriously harmed its own credibility by acknowledging Monday that it had posted the new guidance “in error”, following a pressure campaign from the WHO.
Scientists have been gathering evidence that the novel coronavirus plaguing the world spreads via aerosol particles practically since it first emerged, and back in July, a group of 200 scientists sent a letter to the WHO urging the international public health agency to change its guidance on the spread of the disease. The problem scientists argued is that the WHO hasn’t updated its views to incorporate new research showing that aerosol spread is a much greater threat than touching contaminated surfaces, or via large droplets spread by close contact between individuals.
Yet, the WHO has refused these overtures, and this week it successfully convinced the CDC to do the same.
After the WHO announced earlier that it had reached out to the CDC over the guidance change, the agency informed American media outlets that a “draft version” of the guidance had been “posted in error”.
- “A draft version of proposed changes to these recommendations was posted in error to the agency’s official website,” the CDC said. “CDC is currently updating its recommendations regarding airborne transmission of the coronavirus. Once this process has been completed, the update language will be posted.”
Even so, the American media has grown increasingly convinced that aerosols significantly contribute to overall spread of the virus, with ABC News suggesting yesterday that expensive UV-light powered surface cleaners were merely examples of “hygiene theater”.
For months, the CDC has insisted that these large droplets are the primary mode of transmission, which is why – it argued – people must wear masks in public, because masks are effective at blocking large particles.
However, masks – at least, homemade clothe masks with imperfect seals – aren’t as effective at filtering all aerosol particles. Furthermore, research suggests aerosol particles released when a person sneezes can reach up to 26 feet.

https://zh-prod-1cc738ca-7d3b-4a72-b792-20bd8d8fa069.storage.googleapis.com/s3fs-public/inline-images/NEEZE.png

Source: WSJ

Experts quoted in the US press reports are already slamming the CDC for injecting more confusion into the conversation surrounding C19 prevention at a particularly risky time. After all, schools are still reopening across the US and many are diving headlong into the unknown, fearful that all of this activity could cause another wave of the pandemic, as Dr. Scott Gottlieb warned yesterday.
The FDA is already under fire for its allegedly “premature” approval of convalescent plasma, which critics claim is the result of untoward political pressure from the president. On Friday, the CDC also abandoned controversial guidance saying not everybody who comes into contact with an infected person needs to be tested, and that tests should only be required for those experiencing symptoms [Note: See Next Story].

Source: In Stunning Reversal, CDC Says It Published New Guidance On Risks Of ‘Airborne’ COVID-19 “In Error”

2. CDC reverses controversial coronavirus guidance that said people without symptoms may not need a test

The Centers for Disease Control and Prevention on Friday reversed controversial coronavirus testing guidance that said people who were exposed to an infected person but weren’t showing any symptoms did “not necessarily need a test.”
The new guidance said that people without symptoms who have been in close contact with an infected person “need a test.” The CDC defines “close contact” as being within 6 feet of a person with a confirmed C19 infection for at least 15 minutes.
“Please consult with your healthcare provider or public health official. Testing is recommended for all close contacts of persons with coronavirus infection,” the new guidance said. “Because of the potential for asymptomatic and pre-symptomatic transmission, it is important that contacts of individuals with coronavirus infection be quickly identified and tested.”
Numerous studies have shown that people can carry and spread the virus without showing symptoms — both in the presymptomatic stage and in cases where they never develop symptoms. Public health specialists and officials at the World Health Organization have repeatedly emphasized the importance of testing people who don’t have symptoms in order to cut off chains off transmission.
Many public health specialists criticized the CDC’s change in testing guidance in August for appearing to downplay the significance of testing people who don’t have symptoms but who might be spreading the virus.
The CDC called the shift in guidance a “clarification” and noted the “the need to test asymptomatic persons.”
Representatives from the Department of Health and Human Services, which the CDC falls under, referred CNBC’s request for comment to the CDC.
Dr. Robert Redfield, director of the CDC, sought to clarify the old guidance last month, saying in a statement that “testing may be considered for all close contacts of confirmed or probable C19 patients,” but he stopped short of recommending it for those without symptoms.
“Everyone who needs a C19 test, can get a test. Everyone who wants a test does not necessarily need a test; the key is to engage the needed public health community in the decision with the appropriate follow-up action,” Redfield said in the same statement last month, adding italics in the written statement for emphasis.
Redfield told lawmakers earlier this week that his clarification “didn’t solve the problem” and added that the agency was planning on updating the guidance this week and issuing a clearer clarification. He also said the guidance was “misinterpreted” and that “we were not trying to limit” testing.
“More tests actually can lead to less cases if testing is linked to public health action,” Redfield said Wednesday at the hearing hosted by the Senate Appropriations subcommittee.
The new guidance advised people awaiting test results to “self-quarantine/isolate at home and stay separated from household members to the extent possible and use a separate bedroom and bathroom, if available.”
The updated guidance also said that people who don’t have symptoms and who have not been exposed to an infected person “do not need a test unless recommended or required by your healthcare provider or public health official.” The previous guidance definitively said that such people do not need to be tested.
The updated guidance from the CDC comes amid heightened concerns of political intervention by the White House inside the nation’s premier health agencies, including the CDC and the Food and Drug Administration. At the center of such concerns is Michael Caputo, a former Trump campaign official who was appointed earlier this year as the top spokesman for HHS in a move seen by many to align public health messaging with that of the White House.
Caputo and his allies reportedly meddled with internal CDC affairs, including the publication of the agency’s Morbidity and Mortality Weekly Reports. Those serve as the main channel through which the CDC communicates with physicians and public health specialists across the country about trends and emerging health issues.
HHS announced earlier this week that Caputo will take a 60-day leave of absence. The agency also announced that one of Caputo’s allies, Paul Alexander, who reportedly tried to influence what White House coronavirus advisor Dr. Anthony Fauci said in media appearances, will leave HHS.
The old CDC guidance, which was heavily criticized by health officials, including the former Director of the CDC Dr. Tom Frieden, was posted to the agency’s website in August despite objections from scientists within the CDC, The New York Times reported earlier this week, citing several people familiar with the matter as well as internal documents.
“That was a doc that came from the top down, from the HHS and the task force,” a federal official with knowledge of the matter told the Times. “That policy does not reflect what many people at the CDC feel should be the policy.”
Adm. Brett Giroir, an assistant secretary for health at HHS who is in charge of the federal government’s testing efforts, defended the previous change in guidance last month on a conference call with reporters. He insisted that there was no “weight on the scales” from senior officials at HHS nor from the White House.
“Let me tell you, right up front that the new guidelines are a CDC action,” he said, adding that members of the White House coronavirus task force, including Fauci and Redfield, discussed and agreed on the new guidelines.
But Fauci, who at the time was recovering from a vocal cord surgery, later said that he “was under general anesthesia in the operating room and was not part of any discussion or deliberation regarding the new testing recommendations.”

Source: CDC reverses controversial coronavirus guidance that said people without symptoms may not need a test

H. The Road Back?

1. As more local lockdowns begin, the hard truth is there’s no return to ‘normal’

Opinion by Devi Sridhar, Chair of Global Public Health at the University of Edinburgh

Rather than tell you comforting lies and what you want to hear, I’m going to tell you some unpleasant truths. The world has fundamentally changed over the past nine months since a small pneumonia cluster was reported in Wuhan, China. The “normal” version of reality does not exist anywhere in the world, even if politicians or snake-oil pseudo-scientist salesmen try to persuade you otherwise. If you are struggling with how to cope, know that the only certainty about the year ahead is uncertainty.
As we are witnessing in the UK, restrictions can change quickly as the government grapples with how best to control the spread of the virus with minimal economic and social harm in the process. Every country across the world has some sort of restrictions in place. Yes, even Sweden. The narrative of lockdown and release is no longer helpful as we move into a future of varying degrees of restriction.
As a scientist, I’m often asked what to do and what not to do, and how to cope in this new uncertain world. Here is my advice on how best to enjoy life and get as much normality back while being a responsible citizen.
My main advice is to get outside as much as possible when seeing other people. Research has shown that 97% of “super-spreading” events occur indoors, and that outdoor transmission is minimal. If an indoor setting is poorly ventilated, crowded and no one is wearing face coverings, it is best to avoid it. The upshot is that non-essential shops, outdoor hospitality and public transport look relatively safe with the use of face coverings. Now is the time to avoid non-essential travel and to visit nearby parks, and support your local businesses.
It goes without saying that with a virus that spreads from person to person, the more contacts you have, the more likely you will have to isolate because one of them tests positive. How many people are you in close contact with each week? This means people who you are in physically close contact with for an extended period of time (more than 10 minutes) at close range. Quality of interaction over quantity of contacts is a good rule to follow.
For those who are younger, it is tempting to just want to have C19 and get it over with. But the coronavirus is a nasty virus that you do not want to get. There have been a number of cases of reinfection with the second infection sometimes being asymptomatic or mild, or, in at least one case, being much more serious and requiring hospitalisation. Just because you have it once does not guarantee you immunity for life.
Worryingly, some people aged 30-59 are suffering for months, with horrible fatigue, lung damage and cardiac problems all being described as “long Covid”. The real story of C19 may not be just the lives lost, but the associated disability in younger working-age populations and the burden this places on the economy and health services. Why risk potential decades of ill health instead of putting up with a few months of inconvenience?
As well as the risk Covid poses to individuals, our actions affect others including vulnerable and elderly people. Think of it as a chain of infections – if you are a part of this and it gets passed on, others may become ill and die because of your role in that chain. A wedding in Maine resulted in more than 170 people contracting the virus, and seven people dying. None of those who died attended the wedding.
The only alternative to more restrictions and modifying our own behaviour is a functioning test-and-trace system. Lockdown just presses pause on the spread of the virus. Once restrictions are lifted and governments have pressed play, it will start spreading again. The key objective of lockdown should be to carry out mass testing and tracing in order to aggressively seek out and eliminate community transmission of the virus (like China, Taiwan, Vietnam, New Zealand and South Korea have done). This also buys time for science to develop solutions (such as dexamethasone), and to build healthcare capacity. Simply to lock down for two weeks would be less effective: it is kicking the can down the road.
Nine months after South Korea and Senegal started building diagnostic capacity, it is comically depressing that the UK government, one of the richest in the world, does not have a functional testing system that returns results within 24 hours. In addition, given that we know the virus spreads easily through households, those who test positive should have the offer to isolate in external facilities (such as hotels). The “14-day isolation” measures for people entering the UK are also a box-ticking exercise where given the lack of screening or monitoring, a constant stream of infections keep coming into the country. It’s like trying to empty a bucket under a tap.
The UK government also needs a long-term economic strategy, especially for riskier sectors such as hospitality and bars. The “eat out to help out” scheme has been linked to the rise in cases: the government directly subsidised one of the riskiest settings, indoor hospitality. Instead the money could have been used for economic support packages for these businesses. What will happen to them once new restrictions are brought in? We’re taking one step forward, five steps back.
This is an incredibly hard time for most people. It is perfectly normal to grieve for our lost normality, but denial needs to be followed by acceptance. It is time for governments to plan several years ahead with an acknowledgment and honesty about the severity of this crisis. And for each of us to be patient and compassionate, and take things one day and one week at a time.

Source: As more local lockdowns begin, the hard truth is there’s no return to ‘normal’ | Devi Sridhar

I. Back to School!?

1. The College Freshman’s Life This Fall: ‘Definitely Weird’

On one of his first nights of college, 18-year-old Jamie Gassman joined a poker game.
He and five other first-year students at Whitworth University in Spokane, Wash., sat around a table.
Not at the table. Around it, chairs pushed back so they could be 6 feet apart. One by one, they would stand, approach the table to bet or play a hand, then return to their seats. They wore masks and gloves.
It was a blast, Mr. Gassman said.
Rites of passage for many college freshmen—staying up late in a dorm lounge as strangers turn into friends; sitting alongside hundreds of others for an intro-level class; wandering frat row in a throng of 18-year-olds; tailgating for a football game—aren’t an option this fall, due to the coronavirus pandemic.
Roughly 1,300 colleges and universities are operating primarily or fully online this fall, while about 800 are primarily or fully in person, according to College Crisis Initiative, a tally of schools by Davidson College. Another 650 or so set out to offer hybrid instruction.
Some schools that intended to bring students back have retreated to online instruction amid C19 outbreaks. Others are pushing through despite case counts topping 1,000 in the first weeks of classes.
To move into dorms, some students had to sign pledges they wouldn’t be around anyone besides their roommates without a mask on. Orientation and activity fairs went online. Intramural sports, and some varsity programs, are sidelined. Serendipitous dining-hall meetings are out.
Some who had dreamed of finding independence at school are transitioning into adulthood from their teenage bedrooms.
“Literally every single thing about attending a university is different this year,” said Laurie Leshin, president of Worcester Polytechnic Institute in Massachusetts.
Her campus greeted students with welcome kits including masks and a thermometer and is testing them for C19 at least once a week. It doesn’t allow visitors in residence halls, and students are taking classes in-person and online, limiting opportunities for social interactions.
Mr. Gassman is the first in his family to go to college. Though he could have taken classes remotely, he was eager to be on campus to get what he considered the full experience. Online classes during spring of his high-school senior year weren’t that engaging, he said, plus he had been recruited to Whitworth as a swimmer and wanted to get to know the team.
Now, he is just trying to follow the rules about when to wear masks and how to eat in the dining hall in order to not be sent home.
Dahlia Low, 18, had fallen in love with Barnard College during a campus visit. “The minute I got on campus, I was like, ‘This is the school I have to be at,’ ” she said. “Everything about it felt like me and felt safe and felt welcoming.”
When it admitted her in the spring, she screamed with joy. Then in August, five days before she was supposed to head to Connecticut from her California home to quarantine at her aunt’s house before moving onto campus, as per New York state rules, Barnard notified students fall term would be online only.
Ms. Low outfitted the small guesthouse in her family’s Los Angeles yard with gear she had planned to use at her dorm, so she could at least move out of her bedroom. She spends her days on Zoom, with classes including psychology, American literature and European history.
Nearly all her high-school friends have moved away to be at or near their colleges. “Jonathan, my 4-year-old brother, is currently my best friend,” Ms. Low said, laughing. “It’s definitely weird.”
Her image of college was colored by the movie “Pitch Perfect,” in which the main character stumbles across, then joins, an a capella group at an activities fair. “I’m not getting the chance to have that unexpected experience,” Ms. Low said. “There’s no opportunity for serendipity when every interaction requires a phone call or text message.”
Feeling lonely, she connected with another Los Angeles-based student from her art-history class. They arranged watch the movie “Bridesmaids” together at a drive-in theater.
Luke Halverstadt, 18, started college by flying from New York to New Orleans and spending two days alone in a hotel room awaiting C19 test results.
He moved into a Tulane University dorm, where he and a roommate share a bathroom with a student who has a single room. He isn’t allowed to enter other residence halls; he and his roommate are each allowed one guest, for a total of four people in the room. The school said they are supposed to wear their masks when there are others present.
Half of Mr. Halverstadt’s classes are in person, the other half online.
“I was really excited to meet lots of new people and go out on the weekends,” he said. “That’s really difficult now, and kind of irresponsible.”
His social circle is limited mainly to people from his dorm floor. They have hit up local restaurants and took a kayak trip. He has played volleyball, masked. He said he has seen beer-pong games at a nearby park, students crowding together unmasked.
Tulane said it has disciplined some students for breaking school rules, including gathering in groups of more than a half-dozen in dorm rooms.
“Anything other than sitting in my dorm room carries varying levels of health risks for myself and my community,” Mr. Halverstadt said, “and the weight of that always being on my mind makes it hard to feel as free or independent as I would like.”
Nestor Rodriguez-Garcia, 18, got a taste of independence, moving in early to North Carolina State University and living there for about a month before it sent him home because C19 cases spiked on campus.
Mr. Rodriguez-Garcia, a political-science major, said he was eager to meet new people after growing up in the small coastal town of Calabash, N.C., where he stood out for being Hispanic and politically liberal.
“I came to campus,” he said, “and I met Indian people, East Asian people, people of all cultures.”
Then the outbreaks began, with clusters in multiple residence halls and off-campus housing. Some others from his 10-person suite rented an apartment near campus to continue online classes, but it was too expensive for him.
Mr. Rodriguez-Garcia moved back home and has picked up shifts at a restaurant where he worked in high school to save for a new laptop. His broke, and he logs into Zoom classes on his phone. “I’ll put it very bluntly,” he said: “It kind of sucks.”
One upside: He has privacy. No more college roommate, and his twin brother with whom he had shared a room is still on campus at Western Carolina University.
“I’ve never been in a room by myself,” he said.

Source: The College Freshman’s Life This Fall: ‘Definitely Weird’

2. Forget Zoom Kindergarten. Put Kids Back in School

When it comes to C19, I try not to be judgmental about the choices of others, except to note that anyone who takes fewer precautions than I do is irresponsible, and anyone who takes more than I do is ridiculous. Perhaps you feel the same way. That’s one reason we find it so hard to agree on a way forward on the novel coronavirus, even putting aside our fights about Donald Trump. I may think it’s acceptable to take the risk of going to dinner at a friend’s house; you may not. I’ll try to keep that in mind as I make a case for reopening primary schools across the board. If I happen to feel that keeping them closed is a destructive policy, fed by scaremongering media and boneless public officials, I won’t bang on the table about it. Nobody asked me; I’m under 70; and it’s not Thanksgiving. But I will try to explain why, despite all the confusing data, the case for reopening elementary schools is so strong.
Lest you think I’m in some truther camp or another, let me first establish my credentials as a COVID alarmist. When news of the coronavirus first came out of China, in late January, I took it with all the calm of Fay Wray meeting King Kong. Memories of being in China during SARS in 2003 came roaring back, and I rushed to the hardware store to buy N95 masks (that was then) and to the drugstore to buy sanitizers of every sort. When I went on a family ski trip in February, I brought rubbing alcohol with me everywhere and aimed it at every menacing surface, like a deputy in Tombstone. I wrote an early article fretting about the danger and stocked up on dried and canned goods. By early March, when it became clear that Seattle, where I live, had been experiencing community transmission for weeks, my wife and I pulled our daughter out of third grade. When it became a matter of when, not if, schools would close, I booked an Airbnb on five rural acres and got the family out of town for a while. Call me wise or contemptible, depending on your tastes, but I wasn’t complacent.
Today we all know more. While I don’t regret taking the actions I took—the potential of black swan events must be respected—most of them turned out to be unnecessary. As COVID shut down society, I read a lot of studies and began noticing common threads in super-spreading events: indoor settings, loud voices, crowding. As the months passed, I also observed who seemed to be doing better than expected: grocery workers, flight attendants, and outdoor mass protesters. It became clear that COVID, while contagious, isn’t the measles, racing through populations like a fire through straw, or the bubonic plague, sparing only a fraction of those afflicted. Yes, it can be deadly, especially if you’re exposed to a high dose or you’re weakened by age or comorbidities, but distance and ventilation go a long way. Loud bars are dangerous, but you have to work hard to get infected outside. At this point COVID has become like a grizzly or shark: dangerous enough to be respected, unpredictable enough to kill for no good reason once in a while, but understandable enough to be handled without resorting to bunkers.
This brings us to the matter of schools. While I was among the first to pull my kid out of school, I’d also be among the first to put her back in. That’s because everything we’ve learned about young children and C19 suggests that she’d be fine and so would everyone around her—classmates, teachers, parents. Not only do the vast majority of children under 12 suffer only minor effects from this ailment, but they also tend to keep it to themselves. I’ll return to these points in detail, because specifics are of the essence. But for now my confidence does me no good, as every public school in Seattle remains closed to in-person instruction. The same is true of public schools in Portland, San Francisco, Los Angeles, Chicago, Boston, Washington, D.C., and other cities and counties all over the country. New York City is a laudable exception, if its plans to reopen schools ever translate into real life. But the safety policies New York has put in place make no apparent distinction between high school kids, who seem to be present a high risk of transmission, and elementary school kids, who do not. While hybrid models of remote and in-person instruction are sensible for teenagers, they seem unnecessary for kids under 12, who should be able to go to school pretty much as before.
Let me start by taking the side of the remote-learning faction and present the best case I can for closing elementary schools. Keeping schools closed is just common sense in a deadly pandemic. First of all there’s the danger to the kids themselves. While COVID hits the elderly hardest, about 10% of COVID cases have been among those under 19. Some of those kids have died, and some of those who recovered have experienced frightening aftereffects, most severely in the form of MIS-C, or multisystem inflammatory syndrome, which can involve persistent fever, a rash, damage to the heart, shock, and even death. Second, there’s the danger of transmission. We’ve seen COVID spread in schools in Israel, at summer camps here, and in other places where kids have clustered. That in turn could lead to transmission among adults, adding to an already-terrible mortality rate. Until rates of COVID are vanishingly low, or we have a vaccine, we must avoid settings such as crowded classrooms. Safe is better than sorry.
All of that might sound reasonable enough. I was an early school-avoider myself, after all. But does it apply today? As of September 16, 2020, according to the CDC, 92 children under 18 have died of C19 since February 1 of this year. In that same stretch the flu has killed 123 children, and ordinary pneumonia has killed 313. Over 19,000 children have died of other causes. When it comes to hospitalization rates for children, they are no higher among those with C19 than among those with the flu. Children who have died of C19 seem already to have had serious health problems. For instance, a recent study from England of 651 people under 19 who got sick enough to be admitted to the hospital—meaning cases of already-exceptional severity—found that six died, all of whom “had profound comorbidity.” This is echoed by a CDC statement: “Of the children who have developed severe illness from C19, most have had underlying medical conditions.”
And what about MIS-C, the deadly mystery disease? You might have read New York Times headlines like “15 Children Are Hospitalized With Mysterious Illness Possibly Tied to C19” and “A New Coronavirus Threat to Children,” among others. All of that is scary. At the same time, some perspective is due. At the start of this month, there had been 792 pediatric cases of MIS-C in the United States, leading to 16 deaths, according to the CDC. That is out of more than 500,000 cases of COVID among children in the United States. In other words, fewer than 0.16% of kids with confirmed cases of COVID have developed MIS-C. Those who died of it made up 2% of that 0.16%, meaning the other 98% of that 0.16% recovered. In sum, even if your child is unlucky enough to contract COVID, the odds of him or her developing MIS-C and dying of it would be roughly under 1 in 30,000. That is lower than the odds of being murdered in a year.
All right, let’s go back to the imagined school-closing advocates and allow them to concede some of these points but bring up some others. Fine, they might say. It’s true that we don’t close schools to prevent seasonal flu, or to prevent school-transportation-related deaths (which average over 100 per year). It’s also true we didn’t close schools in 2009 and 2010 when we went through the H1N1 pandemic, which has been estimated to have killed over 1,000 people under 18 in the United States. But COVID is deadlier and more infectious. So far only just over half a million kids have contracted the novel coronavirus, and already 92 are dead. We have some 73.5 million more children to go. If all of them were to get infected and die in the same ratio, over 13,000 of them would perish. Even a quarter of that number is unacceptable. That’s to say nothing of all the adults who would also be killed.
All of which might sound fair enough. But this gets us to part two of the argument: about whether classrooms would trigger a tsunami of transmission. Now, if scholars were united on an answer, we wouldn’t be bickering so much. But so far nearly all of the evidence we have—or at least that I have seen, and I’ll share a lot of it—is consistent with the theory that children under 12 spread COVID only in rare cases.
I first became aware of this when reporting on Sweden, which back in April was defying the world in its eschewal of lockdowns. Sweden had closed schools for older kids, but schools for children under 16 stayed open. The reason, Swedish infectious disease specialist Johan Giesecke explained to me, was that children appeared to be negligible spreaders of coronaviruses. This is in contrast to influenza viruses, which children spread like crazy. Intrigued, I began to look at the literature, and, yes, already by late March we were seeing studies suggesting kids were not major transmitters within households. (The same had been true with SARS.) The “index cases,” meaning the first people in a cluster to get ill and give it to others, tended to be adults, and when kids passed on COVID, it was not to many people.
So what happened in the months that followed in Sweden? According to a report from Sweden’s public health agency, up until June 14, only about 0.05% of the total number of children in Sweden aged 1-19 were diagnosed with C19. That’s a rate no higher than that of neighboring Finland, which went into lockdown. As for other countries with schools that are open, like Germany, Denmark, Japan, and France, the short story is that none has seen a surge of school transmission of C19—with almost no cases, as far I can find, of transmission by children under 12. As WHO chief scientist Soumya Swaminathan said back in May, “There have not been many cases described of children transmitting it to others, particularly within school settings.”
Once again, though, I will take up the voice of the opposition. Unlike the United States, countries that have reopened their schools have beat back their infection rates to low levels. If students at schools aren’t spreading C19, it’s because there’s so little C19 to spread. As it happens, researchers in Spain found that younger kids transmit the disease as much as older kids, and researchers in South Korea found that older kids spread it as much as adults. Plus, think of all the examples of pediatric spreading, like the summer camp in Georgia or the outbreaks in Israel. This points to everyone being a spreader, kids included.
Okay, voice of opposition, that’s a lot of points. But I’ll address all of them. Let’s start with the contention that low infection rates are a precondition for successful school reopenings. It is contradicted by the example of Sweden, where schools stayed open, without leading to any significant pediatric transmission, even as the crisis was at its peak. It’s also undermined by data from the United States, where, over the past several months, tens of thousands of children of frontline workers got placed in childcare centers as the case count was piling up. Spreading in those childcare centers was negligible. Or consider New York. By the time it closed its schools in March, transmission had become rampant among adults, yet we saw no stories of school-centered outbreaks. Cases are rising in France, but schools have reopened all the same, without any indication that it’s causing a spike in cases. Now, it’s not that kids never pass on C19. But the numbers suggest that they spread it only rarely and narrowly.
The next couple of paragraphs are for those who feel like getting most in the weeds, and that may not include every reader, but I’m going to go there, because it’s important. The study in Spain noting that little kids and big kids seem to spread the disease with equal ability is important, but mainly because of its primary point: Regardless of their age, kids in Spanish summer camps barely spread the coronavirus. Researchers collected samples from over 2,000 summer camp participants, among them 30 pediatric index cases, meaning 30 kids who were the first to get sick. Of those 30, only 8 passed anything along to anyone else, while 22 kept their COVID to themselves. All in all, 12 other kids got sick. At that rate of spreading, COVID would vanish in months. As for the finding that younger kids spread C19 as much as older kids, perhaps, but a sample of eight is small.
The Korean study, which looked at 5,706 index cases, seems to offer more reliable numbers on the difference between younger and older kids. It looked at 29 C19-positive children under 10 years old and tracked down 237 of their contacts, including 57 people living with them under the same roof. Those 29 kids got a total of five people sick, less than 0.2 people per child, and three of those people were living with them. Among the 180 non-household contacts of these 29 children, only 2 contracted the virus. Even among the older kids between 10 and 19, the spreading was confined almost entirely to the home. Outside of their homes, however, among 226 contacts, only 2 tested positive. (Of course, the New York Times headline was bound to be “Older Children Spread the Coronavirus Just as Much as Adults, Large Study Finds,” but that’s the Times. We’ll get to that.) In short, if you’re a teacher in a large room with one nine-year-old student who has COVID, your odds of catching anything are going to be remote, let alone your odds of becoming severely ill.
Unfortunately, while the Korean study is valuable to those arguing that children under 10 ought to be in school, it’s of limited use to those trying to figure out what to do with kids between childhood and adulthood. Perhaps kids in the range of 10 to 19 are monolithic in their spreading capacity. More likely, though, is that children gain in capacity to spread the coronavirus as they grow older, reaching parity with adults once they’ve been through puberty. This would mean a 10-year-old is not much different from a nine-year-old, while a 15-year-old is quite different from an 11-year-old. Now, let me concede: This is a theory. But it is one that a lot of specialists seem to embrace, and causes what we’ve been observing to make sense.
This brings us to those ugly cases of spreading in Israel and Georgia. In Israel the major incident of spreading occurred among teenagers in a high school, not, according to anything I’ve read, among children in a primary school (although initial coverage of the matter made this hard to discern). In the case of the summer camp in Georgia, the likeliest direction of the spread was from staffers to kids, not from kids to kids or kids to adults. Moreover, while I hate to be harsh, that summer camp did things so wrong—like cramming people together in unventilated rooms for singing and sleeping—that I almost got COVID just reading about it. [NOTE: Our understanding was that the windows were closed to allow air conditioning in the rooms] If you want to maximize the chances of the disease spreading from child to child, that’s how to do it.
Now, if any of these assertions seem eccentric or unfamiliar, it’s probably because so much of the coverage of the problem has been irresponsible and incomplete. You would think that in a pandemic, which requires a response that encroaches on so many of life’s liberties and pleasures, journalists would sometimes question the utility of restrictions rather than question only their absence. Instead we get a mountain of coverage about what might (just might) be dangerous and very little about what is safe. This can lead people to think everything is dangerous or nothing is. You can find churchgoers who think they’re safe just because they have masks on indoors, when in reality joining a group of adults without ventilation is always going to be a big gamble, or city pedestrians who think they’re at risk from bare faces outdoors, when any exhalations are fast dispersed into the near-infinitude of the troposphere. It’s no wonder that people are confused about what should happen with children.
So let’s make it simple: Young ones should be back in the classroom. Look, I don’t kid myself into thinking I’ll cause major changes of heart, not least since I’m appealing to the head. Most fears, including my own, are outside the realm of logic. I won’t spend the night in a cemetery, no matter what the statistics say. Human nature being what it is, some people will find the action of cramming students and teachers into a classroom to be too frightening to contemplate, period. We cannot blame them for feeling that fear. But we can blame those who insist on letting that fear make our decisions for us. They are harming the long-term learning prospects of children, aggravating many teachers, forcing many parents to quit their jobs, and making young people anxious, bored, and depressed. These are certain harms that must be weighed against claims of potential harms from reopening. So yes, we’ll each have our personal COVID safety protocol and act judgmental about everyone else’s. If you wear a mask outside, I can say you’re silly, and if I refuse to dine indoors, you can say I’m hysterical. It doesn’t matter how we feel or what you or I do. But it does matter whether we choose as a society to let our schools stay closed. We’ve hurt our kids long enough, and it’s time for the fearless and fearful alike to grit their teeth and put a stop to it. Ease into things over the course of weeks, if it reassures people, and open the windows and put on fans to be super safe (even if winter coats will be needed for the cold), but get kids back at their elementary school desks five days a week. Class should no longer be dismissed.

Source: Forget Zoom Kindergarten. Put Kids Back in School.

3. France will now run K-5 schools normally even if kids test positive

France’s Education Ministry announced Sunday that classes in pre-school and primary schools (for pupils aged 3-10), would “continue to be held as usual” even if a classmate tests positive for C19.
As of Tuesday, the new rules are to replace current restrictions whereby pupils considered to have been in close contact with an infected person could only return to school if they test negative after staying home for seven days.
The decision comes after the High Council for Public Health advisory board to the health ministry published a notice Thursday stating “children pose little risk of contracting serious cases and of spreading the coronavirus”.
Three weeks into the school year, 89 public and private schools are currently closed under the existing protocol, a small fraction of the total 61,500, although many more classes within other schools have also been suspended.
“Currently, close to 2,000 classes are closed,” Education Minister Jean-Michel Blanquer said Monday. “The new protocol will allow for fewer closures.”
However, the ministry said the current protocol, which include isolating suspected cases, identifying contacts between pupils and possible closures of classes or entire schools would continue to be applied if three pupils in the same class tested positive.
But teachers, who are required to wear masks, will no longer be considered to be “contact cases” if they have been in contact with unmasked pupils testing positive for C19.

Economic justification

With confirmed cases on the rise and Covid-related hospital admissions increasing, unions questioned the motivation for the government decision.
“You can say children pose little risk of spreading the disease, but not that they pose no risk. Otherwise why would the prime minister call on grandparents to refrain from picking up their grandchildren at school?” asks Guislaine David, general secretary of teachers’ union SnuiPP-FSU, in newspaper Le Parisien.
“To relax the rules in this way, while they are toughened everywhere else, is incomprehensible. The only justification is economic.”
Overall C19 figures posted Sunday evening recorded 10,569 new cases with an average infection rate that had increased from 5.6 to 5.7% in the previous 24 hours, consistent with trends of a simmering epidemic in recent weeks.
Hospital admissions were also growing, with 3,894 new admissions 593 in intensive care in the previous week, also matching the slight upward trend.
“The situation remains worrying,” government spokesperson Gabriel Attal said Monday. “Every day shows we must be more vigilant.”

Source: France eases Covid restrictions in primary schools despite rising cases

4. Children have a low risk of C19 and are disproportionately harmed by precautions

The coronavirus pandemic has brought distinct challenges to the care of children and adolescents globally. Unusually for a respiratory viral infection, children and adolescents are at much lower risk from C19 than any other age group. The near-global closure of schools in response to the pandemic reflected the reasonable expectation from previous respiratory virus outbreaks that children would be a key component of the transmission chain. However, emerging evidence suggests that this is most likely not the case. A minority of children experience a post infectious inflammatory syndrome, the pathology and long-term outcomes of which are poorly understood. However, relative to their risk of contracting disease, children and adolescents have been disproportionately affected by lockdown measures, and advocates of child health need to ensure that children’s rights to health and social care, mental health support, and education are protected throughout subsequent pandemic waves.
Evidence from contact-tracing studies suggest that children and teenagers are less susceptible to coronavirus infection than adults; however, community swabbing and seroprevalence studies conducted outside of outbreak settings suggest that infection rates are similar to those in older age groups. Only half of children and teenagers with antibodies against coronavirus have experienced symptoms, and there is growing evidence that there is a broad range of presentations, emphasizing the limitations of community-based prevalence studies based on testing only children with respiratory symptoms. Hospitalization for severe acute C19 in children is rare, but among these pediatric inpatients, respiratory symptoms are more apparent than in infected children in the community (4). Case fatality in hospitalized children is, fortunately, relatively low at 1% (compared with 27% across all ages).
The reason for the lower burden of symptomatic disease in children is not yet clear. Upper airway expression of angiotensin-converting enzyme 2 (ACE2), a receptor for the coronavirus spike protein, increases with age, and higher ACE2 expression correlates with being positive for coronavirus genomic RNA in swabs of upper respiratory tracts from symptomatic children, but not with viral load. An alternative proposal is the absence in children of maladaptive immune responses that lead to acute respiratory distress syndrome (ARDS) in older age groups, but there are likely other unidentified mechanisms.
Understanding the nature of immune responses in children is important given the rare, but potentially severe, multisystem inflammatory syndrome observed in more than 1000 children and adolescents in multiple countries during the first wave of C19. Known variously as pediatric inflammatory multisystem syndrome temporally associated with the coronavirus (PIMS-TS), multisystem inflammatory syndrome in children (MIS-C), or Kawasaki-like disease, the illness presents with persistent fever accompanied, to a variable extent, by gastrointestinal symptoms, rash, and conjunctival inflammation. Laboratory markers of inflammation are very high, and myocarditis is a distinct, and potentially fatal, feature. Children and young people with PIMS-TS are more likely to have antibodies to the coronavirus than evidence of virus from nasal swabs, with presentations usually 4 to 6 weeks after infection. The cardiac involvement initially led to this condition being described as a variant of Kawasaki disease (in which an unknown trigger leads to an inflammatory disease, resulting in coronary artery inflammation). However, a comprehensive case series clearly delineated PIMS-TS from Kawasaki disease, with children who experience PIMS-TS being substantially older and with increased circulating concentrations of ferritin (a marker of inflammation) and D-dimer and troponin (markers of cardiovascular damage), which are rarely seen in Kawasaki disease. A dominant feature of PIMS-TS is myocarditis, transient myocardial dysfunction, and shock, which are present in approximately half of UK and U.S. case series.
In the UK, a Delphi national consensus statement has recently been proposed to guide investigation and management of this condition, which focuses on supportive care and enrolling patients into a specific arm of the RECOVERY randomized controlled trial to evaluate the use of corticosteroids and intravenous immunoglobulin in patients with acute PIMS-TS. Fortunately, fatalities are rare [occurring in 10 of the 570 cases reported to the U.S. Centers for Disease Control and Prevention between March and July 2020, and none of 52 cases in a UK series]. However, the long-term consequences are unknown, and all children and teenagers who experience PIMS-TS require ongoing cardiac review. Proposed mechanisms for this illness have focused on a maladaptive acquired immune response to coronavirus infection, and a dysregulated humoral immune response is suggested by increased antibodies against multiple, non–coronavirus, respiratory viruses in severe MIS-C but not mild MIS-C or acute C19.
Understanding this response is crucial when considering the risks and benefits of immunizing children against C19, should a vaccine become available. Of the vaccines being tested in clinical trials, none have yet been administered to children, with priority instead being given, appropriately, to older age groups. The most advanced candidate, ChAdOX1-nCOV-19 (the “Oxford Vaccine” or “AstraZeneca Vaccine”), is currently in phase 2 and 3 studies that include a pediatric arm for 5 to 12 year olds (NCT04400838), receiving half the full adult dose in this study. However, this study arm is not currently active and will commence enrolment only once the safety profile in adults is more complete. Given the low rates of disease in children, they are likely to be a low priority to receive a vaccine unless it is definitively shown that (i) children have an important role in the transmission of the virus and (ii) the vaccine reduces viral shedding (and hence reduces transmission).
To what extent do children transmit coronavirus? Recent reports that young children acutely unwell with C19 have concentrations of viral RNA in nasal aspirates that are similar to, or higher, than adults raised concerns that their role in transmission may have been underestimated. However, one of these studies compared children within the first week of illness with adults with more than 7 days of symptoms, when viral load is expected to be reduced. Such studies need to be interpreted with consideration of the very low numbers of children with symptomatic C19.
Of greater concern is the possibility that viral shedding could be occurring from asymptomatic children and that, given schools’ “bridge” households, this could create a pool of ongoing viral circulation responsible for introductions of virus to the pupils’ homes and beyond. Understanding this issue is fundamental to resolving what has been an unprecedented global disruption to primary (children of ~5 to 11 years) and secondary (children aged 11 to 18 years) education. Given the near universal closing of schools in conjunction with other lockdown measures, it has been difficult to determine what benefit, if any, closing schools has over other interventions. However, there is some reassurance: Multiple studies of contacts of primary and secondary school children with known coronavirus infection showed minimal onward transmission in schools. Furthermore, after the reopening of primary schools in the UK, only 1 of 23,358 nasal swabs taken from children in June 2020 had detectable coronavirus, giving an estimate of 3.9 cases per 100,000 students. Looked at from another perspective, when household outbreaks of infection have occurred, it appears that children were responsible for only a small minority of household introductions of the virus. Also, recent surveys found that reopening of schools in a number of European countries in April and May had no clear impact on community transmission, with cases continuing to fall in most countries after reopening.
Nevertheless, recent experiences of substantial outbreaks of C19 related to children and teenagers show that there is no room for complacency. In May, an Israeli secondary school was shut shortly after a post-lockdown reopening after the identification of two symptomatic students independently infected with the coronavirus. A subsequent schoolwide testing campaign revealed that 153 (13.2%) students and 25 (16.6%) staff had detectable coronavirus infection, and contact tracing revealed a further 87 cases in non–school attendees. Although formal studies were not conducted to definitively show school-based transmission, potential contributory factors included a heat wave that led to extensive use of air-conditioning and exemptions from face mask wearing, relatively crowded classrooms (with 35 to 38 per class with 1.1 to 1.3 m2 between students), and shared schoolyard and outdoor spaces.
As schools in the Northern Hemisphere reopen after summer holidays, risk mitigation strategies adopted to variable degrees include creating separate cohorts (or “bubbles”) within schools that interact minimally with each other, use of face masks in crowded areas (if not the classroom itself), and regular screening of students and staff. The coming months will provide an invaluable opportunity to identify which of these measures are most effective at minimizing transmission, to generate a standard “best practice” that balances young peoples’ rights to an education with the need to protect the broader community from further transmission. However, it is inevitable that there will be students attending school while infected with coronavirus, and likely there will be some school outbreaks, with the frequency of these events reflecting levels of community transmission. Regardless, it is hard to support the opening of retail and hospitality sectors while schools remain shut, as occurred in many countries earlier this year.
School closures and attendant loss of other protective systems for children (such as limited social care and health visiting) highlight the indirect, but very real, harms being disproportionately borne by children and teenagers as a result of measures to mitigate the C19 pandemic. In the UK, it is estimated that the impact on education thus far may lead to a quarter of the national workforce having lower skills and attainment for a generation after the mid-2020s, leading to the loss of billions of dollars in national wealth. Additionally, there are a variety of other harms to children’s health, including the risk of reemergence of vaccine-preventable diseases such as measles because of disruptions to immunization programs.
There are many other areas of potential indirect harm to children, including an increase in home injuries (accidental and nonaccidental) when children have been less visible to social protection systems because of lockdowns. In Italy, hospitalizations for accidents at home increased markedly during the C19 lockdown and potentially posed a higher threat to children’s health than C19. UK pediatricians report that delay in presentations to hospital or disrupted services contributed to the deaths of equal numbers of children that were reported to have died with coronavirus infection. Many countries are seeing evidence that mental health in young people has been adversely affected by school closures and lockdowns. For example, preliminary evidence suggests that deaths by suicide of young people under 18 years old increased during lockdown in England.
The role of children in transmission of the coronavirus remains unclear; however, existing evidence points to educational settings playing only a limited role in transmission when mitigation measures are in place, in marked contrast to other respiratory viruses. In the event of seemingly inevitable future waves of C19, there is likely to be further pressures to close schools. There is now an evidence base on which to make decisions, and school closure should be undertaken with trepidation given the indirect harms that they incur. Pandemic mitigation measures that affect children’s wellbeing should only happen if evidence exists that they help because there is plenty of evidence that they do harm.

Source: COVID-19 in children and young people | Science

J. Projections & Our (Possible) Future

1. When Will the C19 Pandemic End?

In 1920, a world wearied by the First World War and sickened by the 1918 flu pandemic desperately sought to move past the struggles and tragedies and start to rebuild lives. People were in search of a “return to normalcy,” as Warren G. Harding put it. Today, nearly every country finds itself in a similar position.
More than eight months and 900,000 deaths into the C19 pandemic, people around the world are longing for an end. In our view, there are two important definitions of “end,” each with a separate timeline:
- An epidemiological end point when herd immunity is achieved. One end point will occur when the proportion of society immune to C19 is sufficient to prevent widespread, ongoing transmission. Many countries are hoping that a vaccine will do the bulk of the work needed to achieve herd immunity. When this end point is reached, the public-health-emergency interventions deployed in 2020 will no longer be needed. While regular revaccinations may be needed, perhaps similar to annual flu shots, the threat of widespread transmission will be gone.
- A transition to a form of normalcy. A second (and likely, earlier) end point will occur when almost all aspects of social and economic life can resume without fear of ongoing mortality (when a mortality rate is no longer higher than a country’s historical average) or long-term health consequences related to C19. The process will be enabled by tools such as vaccination of the highest-risk populations; rapid, accurate testing; improved therapeutics; and continued strengthening of public-health responses. The next normal won’t look exactly like the old—it might be different in surprising ways, with unexpected contours, and getting there will be gradual—but the transition will enable many familiar scenes, such as air travel, bustling shops, humming factories, full restaurants, and gyms operating at capacity, to resume.
The two ends are related, of course, but not linearly. At the latest, the transition to normal will come when herd immunity is reached. But in regions with strong public-health responses, normalcy can likely come significantly before the epidemiological end of the pandemic.
The timeline to achieve the ends will vary by location. In this article, we’ll explain the criteria that will be key factors in determining when each is reached. In the United States and most other developed economies, the epidemiological end point is most likely to be achieved in the third or fourth quarter of 2021, with the potential to transition to normalcy sooner, possibly in the first or second quarter of 2021. Every day matters. Beyond the impatience that most feel to resume normal life, the longer it takes to remove the constraints on our economies, the greater will be the economic damage.

The epidemiological end point

Most countries have deferred the hope of achieving herd immunity until the arrival of a vaccine. When herd immunity is reached, ongoing public-health interventions for C19 can stop without fear of resurgence. The timing of the end point will vary by country and will be affected by a number of factors:
- the arrival, efficacy, and adoption of C19 vaccines—the biggest drivers in the timeline to herd immunity
- the level of natural immunity in a population from exposure to C19; in our estimate, between 90 million and 300 million people globally may have natural immunity
- potential cross-immunity from exposure to other coronaviruses
- potential partial immunity conferred by other immunizations, such as the bacille Calmette–Guérin (BCG) vaccine for tuberculosis
- regional differences in the ways that people mix, which will produce different thresholds for herd immunity
Consider the first and most crucial variables: the arrival of vaccines, their efficacy, and their adoption. We see four plausible scenarios for vaccine efficacy and adoption, illustrated in Exhibit 1 [Note: use link to article to review Exhibit 1]. Different combinations of those two factors will drive varying levels of conferred immunity, implying the extent of natural immunity that will be required to reach herd immunity under each scenario. Combinations of efficacy and adoption beyond those shown are possible.
The other variables will also have much to say about the timeline to reach herd immunity are:

Natural immunity to coronavirus.
- Globally, of the approximately 30 million people known to have C19, more than 900,000 have died. The rest have recovered and have some degree of natural immunity to the coronavirus. While there has been at least a few documented cases of reinfection, most experts expect that the majority of those exposed to the virus are immune for some period of time.
- It’s likely that many more infections haven’t been detected. Estimated case-detection rates range from 3:1 to 10:1.That would mean that between around 90 million and 300 million people around the world have some immunity to the coronavirus.
Infection rates vary widely. In some places, such as Mumbai and New York City, subpopulation antibody-positivity rates range up to 50%. But those are likely to be outliers: in most countries, less than 10% (and often less than 5%) of populations test positive for antibodies.
T-cell cross-reactivity to other coronaviruses. Some recent studies suggest that a significant number of people who haven’t contracted C19 have cross-reactivity in specific immune cells (T cells). Most of them gained it from contracting other coronaviruses, which primed their immune systems to react to C19. The degree to which T-cell cross-reactivity actually immunizes individuals hasn’t been proven. If T-cell cross-reactivity provides meaningful immunity, it would offer significant progress toward herd immunity. The prevalence of cross-reactive immunity may vary substantially by region.
Partial immunity because of other immunizations. Studies have shown that countries that require bacille Calmette–Guérin (BCG) vaccinations for tuberculosis correlate with lower rates of C19 infections and related deaths, normalizing for certain key factors (such as epidemic stage, development, rurality, population density, and age structure). Causation hasn’t been proven.
Threshold for achieving herd immunity. The threshold for achieving herd immunity for C19 is the percentage of a population that needs to develop immunity to disease to prevent sustained future transmission. Once the threshold is reached, the whole population is protected. A basic formula for estimating that threshold is one minus the reciprocal of the basic reproductive number.⁷

In practice, a herd-immunity threshold is complicated and varies by setting. The formula relies on several broad assumptions. One is that each member of a population mixes randomly with all other population members. In reality, people mix mostly with others whose patterns of interaction are similar to their own. Subpopulations with fewer interactions have lower thresholds for herd immunity than do those with more interactions. An estimated overall threshold for herd immunity can be lower than it would be if it took into account that subpopulations with fewer interactions might drive down an overall threshold, and that subpopulations with more interactions have disproportionately already been infected.
Several epidemiologists who are building dynamic models of C19 that incorporate the heterogeneity of population mixing are predicting lower thresholds for herd immunity than previously thought. Many models predict thresholds of about 40 to 50%. Other epidemiologists have called into question those hopeful estimates and note that policy should be based on conservative estimates of herd-immunity thresholds until better information is available.

Based on our reading of the current state of the variables and their likely progress in the coming months, we estimate that the most likely time for the United States to achieve herd immunity is the third or fourth quarter of 2021. As we wrote in July 2020, one or more vaccines may receive Emergency Use Authorization from the FDA before the end of 2020 (or early in 2021) and the granting of a Biologics License Application (also known as approval) during the first quarter of 2021.
Vaccine distribution to a sufficient portion of a population to induce herd immunity could take place in as few as six months. That will call for rapid availability of hundreds of millions of doses, functioning vaccine supply chains, and peoples’ willingness to be vaccinated during the first half of 2021. We believe that those are all reasonable expectations, based on public statements from vaccine manufacturers and the results of surveys on consumer sentiment about vaccines.⁷
Herd immunity could be reached as soon as the second quarter of 2021 if vaccines are highly effective and launched smoothly or if significant cross-immunity is discovered in a population (Exhibit 2) [Note: Use link to article to review Exhibit 2]. (For more on the potential for a faster resolution of the C19 crisis in the United States, see “Searching for optimism in the US response to C19,” forthcoming on McKinsey.com.)
On the other hand, the epidemiological end of the pandemic might not be reached until 2022 or later if the early vaccine candidates have efficacy or safety issues—or if their distribution and adoption are slow. At worst, we see a long-tail possibility that the United States could be still battling C19 into 2023 and beyond if a constellation of factors (such as low efficacy of vaccines and a short duration of natural immunity) align against us.
The paths to herd immunity in other high-income countries are likely to be broadly similar to the one in the United States. The timelines will vary based on differences in vaccine access and rollout and in levels of natural immunity—and potentially, in levels of cross-immunity and previous coverage of other vaccines, such as the BCG vaccine. Even as some locations reach herd immunity, pockets of endemic C19 disease are likely to remain around the world, for example in areas affected by war or in communities with persistently low adoption of vaccines. In such places, until herd immunity is reached, C19 might be analogous to measles—not a day-to-day threat to most people, but a persistent risk. If immunity wanes—for example, if booster vaccines are not fully adopted—then C19 could become more widely endemic.
The arrival of herd immunity won’t mean a complete end to all public-health interventions. It’s possible that regular revaccinations would be required to maintain immunity, and ongoing surveillance for C19 will be required. But herd immunity would mean that the emergency measures currently in place in many countries could be lifted.
The pace at which governments relax public-health measures will be critical. Some of those measures (such as full lockdowns and restrictions on certain industries) have significant social and economic consequences, and others (such as testing and tracing), while expensive, don’t. Many governments are employing packages of measures that aim to minimize the number of C19 cases and excess mortality while maximizing social and economic degrees of freedom.

The transition to normal

The second end point of the pandemic may be reached earlier than the first. We estimate that the mostly likely time for this to occur is the first or second quarter of 2021 in the United States and other advanced economies. The key factor is diminished mortality.
Society has grown used to tracking the number of C19 infections (the case count). But case counts matter primarily because people are dying from the disease and because those who survive it may suffer long-term health consequences after infection. The latter is an area of scientific uncertainty, but there is concern that some recovered patients will face long-term effects.
Most countries have made significant progress in reducing the numbers of deaths and hospitalizations associated with C19. Some are close to eliminating excess mortality. Those results have generally been achieved through a combination of moderately effective interventions rather than a single “big bang” (Exhibit 3) [Note: Use the link to article to review Exhibit 3].
A transition to the next normal, in whatever form that takes, will come gradually when people have confidence that they can do what they used to do without endangering themselves or others. Gaining that confidence will require a continuation of the progress made to reduce mortality and complications, as well as further scientific study regarding long-term health consequences for recovered patients. When confidence is restored, people will again fill bars, restaurants, theaters, and sports venues to full capacity; fly overseas (except for the highest-risk populations); and receive routine medical care at levels similar to those seen prior to the pandemic.
The timing of such a transition will depend on the progress toward herd immunity, as previously detailed (since more people with immunity means fewer deaths and long-term health consequences), and on the effectiveness of a country’s public-health response. Transitions will be gradual. They have already begun in some locations and could be well advanced in most countries by the first or second quarter of 2021. Given the interconnectedness of the global economy, country timelines to normalcy are not fully independent of one another.
To achieve that, we will need to see significant progress on the epidemiological end point, including an effective vaccine receiving Emergency Use Authorization approval during the fourth quarter of 2020 or the first quarter of 2021, followed by a smooth rollout and adoption by high-risk populations. Favorable findings on natural and cross-immunity would help accelerate timelines.
Five additional criteria will also contribute to the transition to a form of normalcy—the more of these that are achieved, the faster the milestone is likely to be reached:
- continued improvement by governments in the application of public-health interventions (such as test and trace) that don’t significantly limit economic and social activities
- compliance with public-health measures until we achieve herd immunity
- accurate, widely available, rapid testing that effectively enables specific activities
- continued advancements in therapeutics (including pre- and post-exposure prophylactics) for and clinical management of C19, leading to lower infection-fatality ratios—substantial progress has already been made through a combination of effective drugs, such as dexamethasone and remdesivir, and changes in clinical management
- public confidence that there aren’t significant long-term health consequences for those who recover from C19
Both the epidemiological and normalcy ends to the C19 pandemic are important. The transition to the next normal will mark an important social and economic milestone, and herd immunity will be a more definitive end to the pandemic.
In the United States, while the transition to normal might be accomplished sooner, the epidemiological end point looks most likely to be reached in the second half of 2021. Other advanced economies are probably on similar timetables.

Source: https://www.mckinsey.com/industries/healthcare-systems-and-services/our-insights/when-will-the-C19-pandemic-end#

2. One Bank Expects COVID Herd Immunity To Emerge By 2022

Last week, Bank of America made a rough, back-of-the-envelope calculation that roughly 12% of the US population had achieved COVID herd immunity, far below the 60% threshold that is necessary for the disease to be contained without fresh policy actions, prompting BofA to propose a vision for a world in which we get periodic covid flareups in the coming months, many of which could culminate in fresh lockdowns.
Taking the initial thoughts from BofA, this morning Deutsche Bank published an extensive report analyzing what “Living with Covid” for the foreseeable future would be like (with an emphasis on Asian countries) since – like BofA – the German bank does not see herd immunity emerging as a factor until 2022 for advanced economies, and 2023 for the rest of the world, to wit:
- Although developments on the vaccine front have been promising, there is uncertainty over the uptake of vaccines by the public and thereby the pace of achieving herd immunity, which would better ensure a more full normalization of economic activity. Our baseline forecast now assumes that some economies will achieve herd immunity to C19 in 2022, along with most advanced economies. Other countries are likely to have to wait until 2023 to achieve the same. Risks around these forecasts are evenly balanced.
Another key point that remains lost on many politicians both in the US and elsewhere is that “the tolerance for extended rigorous social distancing appears to be weakening, with new social distancing regulations being in most places milder and imposed for shorter durations. People appear to have learned how to protect themselves and to live with the virus better than during the initial outbreaks, as economic data are proving in some respects more resilient to the virus.”
The bottom line, as we said many months ago, is that having done the calculus most economies are now willing to reopen their economies as the political and socioeconomic hit from lockdowns is far more adverse to the broader population – and especially the youth which is losing jobs by the millions – than enforcing full quarantine with spotty results while hoping to minimize new cases, something which can be seen most vividly in new cases in some countries like Spain and France, has failed to lead to a rebound in new deaths or hospitalizations.

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Finally, reliance on a vaccine as some magic bullet that will magically cure the global economy appears largely misplaced, because as Deutsche notes, “although developments on the vaccine front have been promising, there are concerns about a possible low acceptance by the public of these new vaccines by the public. It may also matter importantly which vaccines are put into commercial production first – they vary significantly in cost and emerging economies could be at a disadvantage in acquiring enough vaccine.”
The bottom line, according to the report’s authors is that until herd immunity has been achieved – some time in 2022/2023, “economies will remain hostage to the virus – shrinking with each new outbreak and expanding quickly as social distancing eases with the subsequent decline in infection risks.”
One can only hope that after the US elections, the political angle of such decision-making will become moot, and policymakers can finally focus on the most optimal outcome without a preference for decisions that leads to who ends up in the White House, but rather what is truly for the benefit of the people.

Source: One Bank Expects COVID Herd Immunity To Emerge By 2022

3. What It Would Take for Herd Immunity to Stop the Coronavirus Pandemic

The concept of herd immunity is at the heart of global vaccination efforts and discussions about next steps in fighting the C19 pandemic and bringing back economies.
For the pandemic to stop, the coronavirus has to run out of susceptible hosts to infect. Herd immunity occurs when enough people in a population develop an immune response, either through previous infection or vaccination, so that the virus can’t spread easily and even those who aren’t immune have protection.
To reach herd immunity for C19, public-health authorities estimate that around 60% to 70% of a given population would need to develop an immune response to the virus. Some epidemiologists and mathematicians now say herd effects might start to kick in before that point, at perhaps closer to 50%, suggesting potential protection could be achieved sooner.
Still, infectious-disease experts adamantly warn against the notion of trying to reach herd immunity to the coronavirus without a vaccine, as the costs on human life would be staggering and it likely wouldn’t happen soon, if at all.
Even with a vaccine, there will still be barriers to achieving herd immunity. “It’s a continuous process,” said Saad Omer, director of the Yale Institute for Global Health. “You could start seeing [an effect] before that threshold, but the other issue is there might still be outbreaks at a smaller level.”
“It’s not like when herd immunity is achieved, we’re not going to have C19,” he said.
Estimates vary widely for where the herd-immunity threshold lies because researchers use a variety of statistical techniques to account for differences in individuals’ likelihood of spreading the virus.
The herd-immunity threshold is mathematically dependent on the infectiousness of the virus, or how many individuals each infected person goes on to infect—called the basic reproductive number, or R0 (R-naught). Scientists calculate the herd threshold using that number and an equation formulated almost 100 years ago by two pioneering Scottish epidemiologists.
Measles, for example, is extremely contagious. It has a basic reproductive number between 12 and 18 and a herd threshold of 90% to 95%. For SARS-CoV-2, the basic reproductive number is estimated at around 2.5 to 3, implying a herd threshold of 60% to 70%.
But the classic equation makes an assumption—that everyone is equally susceptible to infection and has the same chance of bumping into every other person, like molecules of gas in a bag, said Justin Lessler, associate professor of epidemiology at Johns Hopkins Bloomberg School of Public Health.
“Which of course is ridiculous. It’s not how the world works,” Dr. Lessler said. The equation gives you a good target for vaccine coverage, but it doesn’t capture the dynamics of an epidemic moving naturally from person to person, he said.
In reality, people live in clusters, interacting only with certain individuals. Age, job, social network and even individual biological responses to infection all affect a person’s place in the spidery web of disease transmission.
Essential workers, for instance, are more likely to get infected than people able to limit interactions with others. If those who are more likely to transmit the virus developed immunity early on, whether through infection or vaccine, it would be possible to start seeing a reduction in transmission earlier, epidemiologists say.
Reflecting these real-world effects in disease models can shift the estimated herd immunity boundary. One group of researchers estimated that threshold for C19 could be as low as 10% to 20%, though many epidemiologists say that is unlikely. Other modelers have estimated it at around 40% to 50%. Christopher Murray, director of the Institute for Health Metrics and Evaluation at the University of Washington, said his group estimates the herd-immunity threshold at between 50% and 80%.
If lower estimates for herd immunity are correct, then governments should consider policies to shield the elderly and other at-risk groups from the virus while relaxing restrictions on everybody else, said Paul McKeigue, professor of genetic epidemiology and statistical genetics at the University of Edinburgh, in Scotland.
But most infectious-disease experts strongly advise against that, as it isn’t clear how governments would shield more vulnerable people from the easily spread pathogen. Those in lower-risk groups can become seriously ill and, on rare occasions, die as a result of the disease. Doctors are just beginning to understand long-term health effects.
“If we’re talking about letting the disease run its course [and] infect large numbers of people, essentially what we’re saying is the public-health system has failed to do its job,” said Nadia Abuelezam, an infectious-disease epidemiologist at Boston College. “We’ll have a lot of death, and we’ll have a lot of morbidity.”
Communities, including some neighborhoods in New York, and even individual families that have been hard-hit by the virus likely do have an elevated level of protection. “But it’s a dangerous thing to base your strategy on,” said Dr. Omer. “There’s still enough tinder to be burned.”
Most places aren’t likely near the point where everyone is protected, even as confirmed global infections surpass 30 million and deaths top 950,000.
And even if subpopulations do develop a level of protective immunity, the virus can easily jump to unexposed pockets, especially if restrictions are relaxed and people potentially start to socialize and travel more, epidemiologists say.
In places where cases have slowed, behavioral changes such as mask-wearing and social-distancing are the more likely explanations for reduced transmission, said Natalie Dean, a biostatistician who specializes in infectious diseases at the University of Florida.
Sweden, for instance, which didn’t implement an aggressive lockdown, still has bans on gatherings of more than 50 people, among other restrictions and voluntary guidelines.
A preliminary survey from the Swedish Public Health Agency in May showed that only 6.7% of people from ages 20 to 64 and 2.7% of those from ages 65 to 95 had antibodies. Sweden also has the highest per capita death rate of its Nordic neighbors.
“At this point, I would not bank on herd immunity in most areas on this planet,” Florian Krammer, a professor in vaccinology at the Icahn School of Medicine at Mount Sinai in New York, said during a panel recently at the online Aspen Ideas health festival.
Another wrinkle: Infectious-disease experts aren’t sure how long immunity to the virus might last, or how often re-infections might occur. Past exposure to other coronaviruses might provide some protection, though any effects of that are unclear.
For diseases such as measles, mumps and polio, herd immunity was achieved through vaccination campaigns. Many say the Food and Drug Administration could authorize a C19 vaccine by year-end, but the rollout will likely be staggered well into 2021, incrementally reducing the susceptibility of the population and building up resistance.
And even when one does potentially become available, there are growing concerns that some Americans won’t want it.
How much of the population needs to get vaccinated to help achieve herd immunity also depends on a potential vaccine’s effectiveness. The FDA has said it would authorize a vaccine with 50% efficacy or better. Some vaccines could require more than one dose to build up a robust response.
The coronavirus is unlikely to disappear completely, public-health experts say. More likely, there will be outbreaks in vulnerable pockets that authorities will work to control, similar to measles, or it could circulate similarly to influenza.
But public-health precautions such as mask-wearing can beat back the virus and, coupled with widely administered vaccines, safely help a level of normalcy return, health authorities say.
“With a combination of a good vaccine together with good public-health measures, we may be able to put this coronavirus outbreak behind us,” Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, told The Wall Street Journal’s CEO Council on Wednesday. “There will be an end to this, and we will be able to get back to normal.”

Source: What It Would Take for Herd Immunity to Stop the Coronavirus Pandemic

K. Practical Tips & Other Useful Information

1. Experts say these are the products to buy before fall and winter

At the start of the pandemic in March, some products seemed impossible to find stocked on store shelves: disinfectant wipes, yeast to make bread, bikes and even jigsaw puzzles sold out as stay-at-home orders swept the nation.
The same thing could happen again in the fall and winter, when there’s expected to be another wave of infections as people spend more time indoors. White House advisor Dr. Anthony Fauci said that Americans should prepare to “hunker down to get through this fall and winter,” in a panel discussion with doctors from Harvard Medical School Sept. 10.
It’s likely that people will return to a similar shopping patterns that they developed early in the pandemic, Kelly Haws, a marketing professor at the business school at Vanderbilt University who specializes in consumer psychology, tells CNBC Make It.
Beyond feeling prepared, there’s a psychological reason why we tend to “panic-shop” in times of crisis. “C19 has forced many of us into circumstances where we feel out of control and uncertain about the future,” Haws says. “Buying stuff that we need in our daily lives is a very easy form of regaining some control.”
Here’s what experts say you should buy now to be prepared for the fall and winter:

Shelf-stable foods

It’s always good to have a two-week supply of essentials such as shelf-stable food and medications that could sustain you and your family in an emergency, Haws says. But it’s important not to overreact and go into panic-shopping mode, she says. Although there were shortages of essential items (such as toilet paper) at the start of the pandemic, eventually those shortages were resolved.
As you grocery shop, make sure you have enough of the less-essential food items that you always incorporate in your routine, Haws says. For example, “I pretty much always make sure I have plenty of coffee on hand, because the idea of not having it just doesn’t sit well with me,” she says.
Investing in small comforts can go a long way: “Have something that makes you continue to feel good and feel like yourself and have a little bit of normalcy, whether that be through particular beverage or food that you like, or through clothing that you wear,” she says.

Cleaning supplies and hand sanitizer

With the next wave of the pandemic coming around flu season, it will be extra important to follow appropriate hand hygiene to prevent the spread of C19 and the flu. But the scarcity of disinfectant wipes has been slower to resolve than some things, like toilet paper.
Sara Skirboll, shopping and trends expert at RetailMeNot, suggests picking up just one extra cleaning item each shopping trip you take. (Most stores also have a limit to the number allowed per customer.) “Then you’re not contributing to the overall shortage when and if that actually happens,” she says. The easy-to-find cleaner Pine Sol was recently approved by the U.S. Environmental Protection Agency because it was shown to kill the virus that causes C19.

Subscription boxes

According to Skirboll, subscription boxes were hot during the last lockdown. It’s a good idea to sign up for a subscription box service now, because there could be delays or wait lists if there is another surge in demand, she adds.
Luckily for parents who are juggling remote learning, there are lots of subscription boxes that are targeted for kids, such as Kiwi Co, she says. (Many can be purchased on Amazon.) Each month, you can receive a box with an educational activity or lesson for kids of all ages.
Signing up for a meal kit subscription boxes, such as Butcher Box or Hello Fresh, can also reduce the amount of grocery shopping that have to do in person, she says. “The neat thing is you’re almost guaranteed that you’re going to be getting some fresh supply of food to your door every month or however often you sign up,” she says.

Exercise equipment

With gyms closed, there was a shortage of home workout equipment, such as free weights, kettlebells and workout benches. Skirboll suggests looking on Facebook Marketplace and Nextdoor Marketplace to see if anyone in your neighborhood is selling gently-used weights or other home workout tools that you can’t find at major retailers.
While it is safer to exercise outdoors during C19, that may be difficult during cold winter months. “Gloves, hats and materials that allow people to exercise outdoors will be very important,” Skirboll adds.

Air purifiers

We know that C19 is spread through respiratory droplets when an infected person sneezes, coughs, talks or breathes. Home air purifiers can filter out the airborne particles in your air that could possibly contain C19, Shelly Miller, professor of mechanical engineering at the University of Colorado Boulder who studies urban air pollution, tells CNBC Make It.
HEPA, or “high-efficiency particulate air” filters have been shown to be very effective at capturing at least 99.97% of airborne particles that are at least 0.3 microns in size, she says. (For context, the C19 virus is about 125 nanometers or 0.125 microns large.) Air cleaners essentially pull air in, pass it through a filter that removes small airborne particles and then dumps clean, particle-free air back in the room, she explains.
While it’s not clear what effect these portable devices would have on C19 transmission, or if ventilation alone can eliminate the virus, increased air circulation is a good idea.
When buying an air purifier, look for a device that uses HEPA filters, and also consider the size of the space you’re hoping to clean, Miller says. The Association of Home Appliance Manufacturers has a great database of air cleaners that have been independently vetted, she adds.

Holiday gifts

Start your holiday shopping even earlier than you would in typical years, Skirboll says. “There are going to be delays and possibly inventory issues, so if you know what you want, go ahead and buy those things as soon as you can,” she says. Especially if you’re buying special toys for kids, because those are likely to sell out, she says.
Another thing about holiday shopping: Black Friday is an unknown at the moment, Skirboll says. With more people shopping online versus in-person, all the more reason to get a jump on your list, she says.

Source: Coronavirus: Why humidifiers, air purifiers may sell out this winter

2. Coronavirus symptoms: how to tell if you have a common cold, flu or Covid

With winter approaching, the UK is entering the traditional seasons for colds and flu, with the additional complication this year that symptoms of those two illnesses can be broadly similar to those experienced by people who have caught the coronavirus and may be at risk of spreading it.
The NHS in England has produced a guide to differentiate between the three types of illnesses, which health experts hope will make it clearer to people whether they have an illness they would have most likely brushed aside last year, but which this year might lead them to think they need to self-isolate or seek to have a coronavirus test.

Coronavirus or Covid-19

The most common symptoms of coronavirus or C19 are a fever – a temperature of 37.8C (100F) – a new persistent cough (usually dry), and a loss of their sense of taste and/or smell. Patients may also sometimes suffer from fatigue, aches and pains, sore throat, headaches and shortness of breath. Diarrhoea and a runny or stuffy nose are rare. The NHS says symptoms can range from mild to severe.

Colds

The most common symptoms of a cold are sneezing, aches and pains, a runny or stuffy nose and sore throat. A mild cough can be experienced. There is sometimes fatigue, and it is rare to experience a fever or headaches. Colds do not cause diarrhoea. The NHS states that with a cold there is usually a gradual onset of symptoms.

Flu

Flu most commonly consists of a fever, fatigue, a dry cough, aches and pains and headaches. Patients will sometimes experience a runny or stuffy nose or a sore throat. Diarrhoea can sometimes occur in children. There is no sneezing or shortness of breath with flu, and the NHS notes there is usually a rapid onset of symptoms.

Source: Coronavirus symptoms: how to tell if you have a common cold, flu or Covid

L. Johns Hopkins C19 Update

September 21, 2020

1. Cases & Trends

Overview

The WHO C19 Dashboard reports 30.95 million cases and 959,116 deaths as of 10:30am EDT on September 21. Last week, the WHO reported more than 2 million new cases, a new weekly record and an increase of 6.5% from the previous week.

Total Daily Incidence (change in average incidence; change in rank, if applicable)

1. India: 91,593 new cases per day (-94)

2. USA: 40,691 (+5,897)

3. Brazil: 30,596 (+3,034)

4. Argentina: 10,922 (+254)

5. Spain: 10,531* (+790)

6. France: 10,381 (+2,336)

7. Colombia: 6,965 (-149)

8. Russia: 5,798 (+469; ↑ 1)

9. Peru: 5,611 (-52; ↓ 1)

10. Israel: 4,547 (+840; new)

Per Capita Daily Incidence (change in average incidence; change in rank, if applicable)

1. Israel: 676 daily cases per million population (+97)

2. Montenegro: 432 (+169; ↑ 1)

3. Bahrain: 412 (+8; ↓ 1)

4. Andorra: 407 (+168; ↑ 1)

5. Argentina: 242 (+6; ↑ 1)

6. Costa Rica: 232 (-8; ↓ 2)

7. Spain: 225* (+17)

8. Czech Republic: 174 (+67 ; new)

9. Peru: 170 (-2)

10. Bahamas: 161 (+22 ; new)

India appears to have passed a peak in terms of daily incidence, reporting more than 93,000 new cases each on September 17 and 18 before decreasing for 3 consecutive days. Mexico fell out of the top 10 in terms of total daily incidence, and it was replaced by Israel. Kuwait and Panama fell out of the top 10 in terms of per capita daily incidence, and they were replaced by the Czech Republic and the Bahamas. Additionally, the Occupied Palestinian Territory is reporting 166 daily cases per million population, which would be #10 in terms of per capita daily incidence if it were a WHO Member State.

United States

The US CDC reported 6.75 million total cases and 198,754 deaths. The US is averaging 40,207 new cases and 794 deaths per day. In total, 22 states (increase of 1) are reporting more than 100,000 cases, including California with more than 700,000 cases; Florida and Texas with more than 600,000; New York with more than 400,000; Georgia with more than 300,000; and Arizona and Illinois with more than 200,000.

The Johns Hopkins CSSE dashboard reported 6.82 million US cases and 199,636 deaths as of 12:30pm EDT on September 21.

2. US CDC TESTING GUIDANCE

Several weeks ago, the US CDC published controversial SARS-CoV-2 testing guidance indicating that individuals with known exposure to C19 cases “do not necessarily need” to be tested. Since then, information has emerged in various media reports that the guidance was drafted by officials at the Department of Health and Human Services (HHS) and the White House Coronavirus Task Force and did not undergo the traditional CDC review process before being posted to the CDC website. On Friday, the CDC published another update that now recommends testing for all individuals with known exposure to C19 cases. The update is very clear regarding individuals who have been within 6 feet of someone with known SARS-CoV-2 infection for at least 15 minutes: “You need a test.” Additionally, the update recommends that individuals with known exposure self-quarantine/isolate for 14 days, regardless of whether their test result is positive or negative.

In the weeks since the previous update, a number of experts have called for this kind change to the testing guidance, particularly in light of the current understanding of the role of asymptomatic and presymptomatic transmission in the pandemic. Notably, we are not aware of any new studies or information since the previous change that significantly affects our understanding of asymptomatic or presymptomatic transmission, so it appears that the most recent update is a correction to the previous guidance.

3. VACCINE SAFETY

Vaccine safety continues to be an object of concern among the public. A poll conducted by the Pew Research Center found that only 51% of US adults would definitely or probably get a SARS-CoV-2 vaccine if it were available, a substantial decrease from 72% in late April and early May. Additionally, 77% of respondents indicated that they expect a vaccine to be approved before its safety and efficacy is fully studied, and 78% indicated that a rushed approval process is their greatest concern regarding the vaccine. More than 90 health organizations issued an open letter to the US FDA to address these fears, encouraging the FDA to complete Phase 3 clinical trials and utilize existing regulatory processes to fully evaluate and authorize a vaccine for public use.

A group of Black physicians from the National Medical Association created an independent expert panel to review data on candidate vaccines and therapeutics with the aim of increasing confidence and uptake of effective medical countermeasures among Black communities who have been disproportionately affected by C19. The National Medical Association was founded in 1895, at a time when Black doctors were excluded from other medical associations, and it aims to eliminate health disparities affecting Black patients. In addition to safety and efficacy data from clinical trials, the panel will also review study design to evaluate the extent to which racial and ethnic minorities are included. The panel hopes its review and recommendation will ensure the appropriate evaluation of candidate vaccines and help improve uptake of safe and efficacious vaccines among Black and other racial and ethnic minorities.

After pressure from health experts to increase transparency regarding their vaccine clinical trials, AstraZeneca, Moderna Therapeutics, and Pfizer disclosed their Phase 3 clinical trial protocols. Study protocols for clinical trials have historically not been made public until after the trial is completed. The study protocols describe how the 3 companies intend to analyze the trial data, including outcomes of interest and conditions that would result in early termination. The studies also describe the points at which preliminary data will be analyzed and the conditions for applying for an Emergency Use Authorization prior to the completion of the trial. AstraZeneca’s protocol is of particular interest after the Phase 3 trials were suspended as a result of a serious adverse event in one of the participants. The trials were resumed in the UK following an independent safety review, but the company has released only minimal information about the event and related data.

4. AIRBORNE/AEROSOL TRANSMISSION

On Friday, the US CDC updated its guidance regarding SARS-CoV-2 transmission, in particular with respect to droplet and airborne/aerosol transmission routes. The update emphasized the role of airborne/aerosol transmission, noting that aerosols are believed to “be the main way the virus spreads” and that “airborne particles” can remain suspended in the air for prolonged periods of time and travel distances beyond 6 feet. This represented a major shift in how the CDC communicated regarding respiratory transmission of SARS-CoV-2, which previously focused on “droplet” transmission (ie, via larger respiratory particles).
This morning, the CDC issued a statement that the information updated on Friday was a draft version of guidance that was published prematurely. The website was updated again today to revert to the previous iteration of the guidance (ie, that emphasizes droplet transmission as the primary route). The current website on SARS-CoV-2 transmission notes that the CDC is in the process of updating its guidance and that new language will be published “once [the] review process has been completed.” If the CDC shifts its focus to airborne/aerosol transmission as the primary concern for SARS-CoV-2, it is unclear if associated recommendations regarding mask use (which are less or minimally effective at reducing aerosols compared to larger droplets), physical distancing, face shields or other solid barriers, or other mitigation measures will change as well.

5. HUMAN/PET TRANSMISSION

A study published in the US CDC’s Emerging Infectious Diseases journal provides further evidence that SARS-CoV-2 can be transmitted between animals and humans, potentially including pets. The study tested 50 cats for C19 in Hong Kong and identified 6 SARS-CoV-2 infections. Based on findings during the 2003 SARS epidemic, Hong Kong initiated a policy of quarantining mammalian pets belonging to humans with confirmed SARS-CoV-2 infection. While the researchers identified 6 feline infections, they were not able to definitively identify specific instances of human-to-animal or animal-to-human transmission.

6. LONG-TERM CARE FACILITIES

Nursing homes and other long-term care facilities provide ideal conditions for the spread of SARS-CoV-2, including prolonged indoor contact and residents at elevated risk for infection and severe disease, and nursing homes account for a disproportionately high fraction of US C19 cases and deaths. Last week, the Centers for Medicare and Medicaid Services (CMS) unveiled the report by an expert panel convened to provide additional recommendations for improving safety at long-term care facilities in the midst of the US epidemic. The expert panel cited increased testing, PPE availability, and increased training and pay for nursing staff as key factors in mitigating the risk. Some patient care advocates have criticized the report for not holding the facilities themselves more accountable for patient safety. In fact, one of the panel members reportedly refused to endorse the report over these concerns.

Researchers at the CDC and the West Virginia Bureau for Public Health published a study in the US CDC’s MMWR that analyzed the odds of a C19 outbreak based on CMS ratings at long-term care facilities in West Virginia. The ratings are based on health inspections, staffing ratios, and 15 “physical and clinical measures,” and each facility is assigned a rating of 1 (lowest) to 5 (highest) stars. In West Virginia C19 outbreaks were reported in 14 of 123 total facilities. The researchers found that the odds of a C19 outbreak in West Virginia facilities rated as 4 or 5 stars were 94% lower than in 1-star facilities, and the odds in 2- and 3-star facilities were 87% lower than in 1-star facilities. Of the 14 outbreaks in long-term care facilities in West Virginia, 7 were 1-star facilities, compared to 5 outbreaks in 3-star facilities and 1 in a 4-star facility*. Statewide, 12% of long-term care facilities were rated as 1 star, but 1-star facilities accounted for 50% of the outbreaks in long-term care facilities.

7. EYEGLASSES

Researchers from China published findings from study investigating whether the use of eyeglasses provides protection against SARS-CoV-2 transmission. The study, published in JAMA: Ophthalmology, included a cohort of 276 hospitalized C19 patients in Hubei Province in January-March. Among these patients, 5.8% routinely wore eyeglasses—defined as more than 8 hours per day—compared to an estimated 31.5% among the general public. The researchers hypothesize that wearing glasses could reduce the amount that people touch their eyes, which could reduce SARS-CoV-2 transmission. While protective eyewear is recommended for healthcare professionals, peer-reviewed evidence is limited regarding any potential protective effect for the general public. Further research is necessary to better characterize any effect of eyeglasses on mitigating SARS-CoV-2 transmission risk outside the context of the healthcare setting.

8. SPORTS

As countries attempt to relax social distancing measures and resume some measure of normal social activity, sporting events seem to remain among the top priorities in many parts of the world. Sports and leagues have taken a variety of approaches to resuming play, and some have faced additional challenges as a result of surging C19 incidence. The French Open (tennis) is scheduled to start later this week, but several players have been forced to withdraw due to positive SARS-CoV-2 tests, including several who had close contact with a coach who tested positive. The tournament will permit 5,000 spectators per day, despite increasing C19 incidence in France, including the Paris area, although this is still much fewer than the 20-30,000 anticipated previously. All spectators will be required to wear a mask. Players will participate in a “bubble,” with dedicated housing and periodic testing throughout the tournament. Following the report of positive tests among players and coaches, some players have expressed concern about how tournament officials are managing the player’s bubble.

College football has resumed in many parts of the US, and more conferences are planning to resume play in the near future. The start of the season has not been without setbacks, however, with multiple games being postponed or possibly cancelled due to C19. The opening game between the University of Virginia and Virginia Tech was postponed after positive SARS-CoV-2 tests at Virginia Tech did not leave enough players to play the game. Similarly, the game between the University of Houston and Baylor University was postponed due to Baylor not having enough players. The head coach for Louisiana State University (LSU) recently reported that “most of [the] players have caught it [C19].” It is unclear exactly how many players have tested positive, at LSU or any other school, but these cases do not appear to be affecting conference plans to continue the season. As we have covered previously, the risk of longer-term health effects remains uncertain; however, evidence continues to emerge of C19 patients experiencing long-term issues, younger and healthier adults that exhibit mild symptoms during the acute phase of their disease.

Despite these events, the Big Ten Conference announced last week that it intends to resume play on October 23-24. Notably, a number of states in the Midwest (where most Big Ten schools are located) are reporting concerning C19 trends, including on college campuses. In fact, several days before the announcement, health officials in Ingham County, Michigan (home to Michigan State University), asked all students to “self-quarantine” for 2 weeks due to a recent increase in local C19 incidence. Interestingly, the guidance recommends that students remain at home except for in-person classes, sports practices, their jobs, medical care, or shopping, which does not sound much like quarantine.

Ten (10) people have been ordered to quarantine following the NFL game between the Houston Texans and the Kansas City Chiefs. The Kansas City Chiefs permitted a limited number of spectators into the stadium for the game, and one subsequently test positive for SARS-CoV-2. The team coordinated with local health officials to conduct contact tracing efforts in order to identify those who may have been exposed.

Index

A. The Pandemic As Seen Through Headlines

B. Numbers & Trends

C. New Scientific Findings & Research

D. Vaccines & Testing

E. Improved & Potential Treatments

F. Concerns & Unknowns

G. CDC Reversals

H. The Road Back?

I. Back To School!?

J. Projections & Our (Possible) Future

K. Practical Tips & Other Useful Information

L. Johns Hopkins COVID-19 Update

Notes:

A. The Pandemic As Seen Through Headlines

B. Numbers & Trends

1. Cases & Tests

Worldwide Cases:

Observations:

US Cases & Testing:

Observations:

2. Deaths

Worldwide Deaths:

Observations:

US Deaths:

Observations:

3. Top 5 States in Cases, Deaths, Hospitalizations & Positivity (9/21)

Observations:

4. Nationwide Trends (9/21)

Observations:

5. 6 Midwest States At ‘Tipping Point’

C. New Scientific Findings & Research

1. Coronavirus Researchers Discover How C19 May Trigger Fatal Levels of Lung Inflammation

2. Bradykinin Storm

3. Children’s immune response against C19 better than adults leads to different theories for treatment and vaccines

4. Discovery of druggable pocket in the Coronavirus Spike protein could stop virus in its tracks

5. Study suggests dengue may provide some immunity against C19

6. The Core Lesson of the C19 Heart Debate

D. Vaccines & Testing

1. Could a Century-Old TB Shot Protect Against C19?

E. Improved & Potential Treatments

1. Vitamin D can help reduce coronavirus risk by 54%

2. A Drug Used to Treat Deadly Coronavirus Infections in Cats May Be an Effective Treatment Against C19

3. Experimental cancer drug AR-12 could be a promising C19 treatment

F. Concerns & Unknowns

1. Stillbirth rate rises dramatically during pandemic

Global trend

Disrupted services

2. Colds Nearly Vanished Under Lockdown – Now They’re Coming Back

G. CDC Reversals

1. In Stunning Reversal, CDC Says It Published New Guidance On Risks Of ‘Airborne’ C19 “In Error”

2. CDC reverses controversial coronavirus guidance that said people without symptoms may not need a test

H. The Road Back?

1. As more local lockdowns begin, the hard truth is there’s no return to ‘normal’

Opinion by Devi Sridhar, Chair of Global Public Health at the University of Edinburgh

I. Back to School!?

1. The College Freshman’s Life This Fall: ‘Definitely Weird’

2. Forget Zoom Kindergarten. Put Kids Back in School

3. France will now run K-5 schools normally even if kids test positive

Economic justification

4. Children have a low risk of C19 and are disproportionately harmed by precautions

J. Projections & Our (Possible) Future

1. When Will the C19 Pandemic End?

The epidemiological end point

The transition to normal

2. One Bank Expects COVID Herd Immunity To Emerge By 2022

3. What It Would Take for Herd Immunity to Stop the Coronavirus Pandemic

K. Practical Tips & Other Useful Information

1. Experts say these are the products to buy before fall and winter

Shelf-stable foods

Cleaning supplies and hand sanitizer

Subscription boxes

Exercise equipment

Air purifiers

Holiday gifts

2. Coronavirus symptoms: how to tell if you have a common cold, flu or Covid

Coronavirus or Covid-19

Colds

Flu

L. Johns Hopkins C19 Update