Coronavirus Update 8-18

Recent Developments & Information

August 18, 2020

Without reliable information, we rely on fear or luck.

“For your country right now and for the war that we’re in against COVID, I’m asking you to do four simple things: wear a mask, social distance, wash your hands and be smart about crowds. I’m not asking some of America to do it. We all gotta do it. If people fail to follow those tips, next season could be “the worst fall, from a public health perspective, we’ve ever had.”
Dr. Robert Redfield, director of the CDC

“‘If carefully done, according to the guidelines, there is no reason why you shouldn’t be able to do that (vote at polling place).’”
President Trump, quoting Dr. Fauci

Index

A. The Pandemic as Seen Through Headlines

B. Numbers & Trends

1. Cases & Tests

2. Deaths

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

L. Johns Hopkins COVID-19 Update (8/17)

M. Links to Other Stories

Robust T Cell Immunity in Convalescent Individuals with Asymptomatic or Mild C19 Coronavirus elicits robust, broad and highly functional memory T cell responses, suggesting that natural exposure or infection may prevent recurrent episodes of severe C19.

Large Study Suggests Convalescent Plasma Can Help Treat C19, but Experts Have Doubts A study, which enrolled more than 35,000 patients, found that quickly administering so-called convalescent plasma had a marked effect on mortality for patients with severe cases of C19. Those who received transfusions within three days of diagnosis had a seven-day death rate of 8.7%, while patients who got plasma after four or more days had a mortality rate of 11.9%. But without a placebo group for comparison, it’s unclear just how valuable the treatment might be.

Plans of US Parents Regarding School Attendance for Their Children in the Fall of 2020: A National Survey

Duration of Isolation and Precautions for Adults with C19 New CDC Guidance For Adults with C19

What day is it? How pandemic stress alters your perception of time Has the C19 pandemic made the passage of time feel strange? Time blindness is a real phenomenon, and it may be more common than ever.

YouTuber’s DIY gun shoots masks onto people’s faces YouTuber Allen Pan decided to create a mask launcher that attempts to shoot masks onto people’s faces. DO NOT ATTEMPT AT HOME!

Sanofi and CVS are building COVID-safe flu vaccination stations Flu season is nearly upon us. CVS, Walmart, Walgreens, and others are moving flu shots outside.

Scientists sound the alarm: Lockdowns may escalate the obesity epidemic Scientists sound the alarm: Lockdowns may escalate the obesity epidemic Emotional stress, economic anxiety, physical inactivity and social distance – locking down society to combat C19 creates psychosocial insecurity that leads to obesity, warn three Danish researchers.

Rapid Testing is at Parties, Concerts and Hotels. Social Distance Still Required. Determined to proceed with parties and events this summer, hosts are adding screenings at the door. But such measures are hardly a guarantee of safety, medical experts warn.

Longitudinal analyses reveal immunological misfiring in severe C19 Researchers have identified a maladapted immune response profile associated with severe C19 and poor clinical outcome, as well as early immune signatures that correlate with divergent disease trajectories.

B. Numbers & Trends

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

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

1. Cases & Tests

Worldwide Cases:

Total Cases = 22,036,889 (+0.9%)
New Cases = 191,865 (-25,061) (-11.6%)
New Cases (7 day average) = 258,088 (-3,326) (-1.3%)

Observations:

Lowest number of new cases since 7/6
7 day average of new cases has been relatively flat since 7/28 (ranging between 262,929 and 253,179) – the only plateau of new cases since the start of the pandemic
1,000,000+ cases every 4 days (based on 7 day average)

US Cases & Testing:

Total Cases = 5,612,027 (+0.7%)
New Cases = 40,612 (2,930) (+7.8%)
Percentage of New Global Cases = 21.2%
New Cases (7 day average) = 50,800 (-1,318) (-2.5%)
Total Number of Tests = 71,687,718
Percentage of positive tests (7 day average) = 7.4%

Observations:

7 day average of cases has been trending down since 7/25
7 day average of cases declined from 69,328 on 7/25 to 50,800 on 8/17, a decline of 26.7%

2. Deaths

Worldwide Deaths:

Total Deaths = 776,869 (+0.5%)
New Deaths = 4,090 (-453) (-10.0%)
New Deaths (7 day average) = 5,680 (-62) (-1.1%)

Observations:

Number of new deaths has declined 5 consecutive days
Lowest number of new deaths since 7/13
7 day average of new deaths has declined 6 consecutive days

US Deaths:

Total Deaths = 158,929 (+0.4%)
New Deaths = 568 (+101) (+21.6%)
Percentage of Global New Deaths = 13.0%
New Deaths (7 day average) = 1,125 (-4) (-0.4%)

Observations:

7 day average of new deaths has been trending higher since 8/8
7 day average of new deaths has increased from 1,027 on 8/8 to 1,068 on 8/17, an increase of 3.8%
Number of new deaths in US fall to 4^rd highest, behind India, Brazil & Mexico

3. Top 5 States in Cases, Deaths, Hospitalizations & Positivity (8/17)

Source: Worldometer and The Covid Tracking Project

C. Updates

1. 7 months later, what we know about C19 — and pressing questions that remain

In the time since Chinese scientists confirmed the rapidly spreading disease in Wuhan was caused by a new coronavirus and posted its genetic sequence on line, an extraordinary amount has been learned about the coronavirus, and how it affects us.
Here are some of the things we have learned, and some of the pressing questions we still need answered.

What We Know

Covid and kids: It’s complicated

Early in the pandemic, it looked like there was a silver lining to the disease cloud sweeping across the world. Children, it seemed, didn’t develop the severe symptoms that were sending adults to hospitals struggling for breath, and they very rarely died. It even seemed that kids didn’t contract the disease at the same rates as adults did.
But everything Covid is complex, and kids are no exception. While deaths among children and teens remain low, they are not invulnerable. And they probably contribute to transmission of the coronavirus, though how much remains unclear.
We’ve learned younger children and teenagers shouldn’t be lumped together when it comes to Covid. Teens seem to shed virus — emit it from their throats and nasal passages — at about the same rates as adults. Kids under 5 have high levels of virus in their respiratory tracts, but it’s still not clear how much they spread it or why they don’t develop symptoms as often as adults do.
A recently published report from a Georgia sleep-away camp shows how quickly the virus can spread among kids. The camp had to be closed within 10 days of starting its orientation for camp staffers, because within days of children arriving, kids and staff started getting sick. (The campers ranged in age from 6 to 19.) The camp did not require campers to wear face masks.
A recent report on Covid infections in children from the CDC showed that while they remain low, U.S. hospitalization rates for C19 in children have risen since the pandemic started. And 1 in 3 children hospitalized with the disease ends up in intensive care. The highest rate of hospitalizations in children was among those under 2 years of age.
Black and Latino children were hospitalized at higher rates than white children. And like adults, children with other health conditions — obesity, chronic lung diseases, or infants who were born premature — are at higher risk than otherwise healthy children.
Perhaps most alarmingly, it’s become clear that a small proportion of children infected with C19 go on to develop a condition where multiple organs come under attack from their own immune system. Called multisystem inflammatory syndrome in children or MIS-C, this condition seems to occur about 2 to 4 weeks after C19 infection. Most children who develop this syndrome recover.

There are safer settings, and more dangerous settings

Research has coalesced on a few key points about what types of setting increase the risk that an infectious person will pass the virus to others.
Essentially, the closer you are to someone infectious and the longer you’re in contact with them, the more likely you are to contract the virus, which helps explain why so much transmission occurs within households. Being indoors is worse, particularly in rooms without sufficient ventilation; the more air flow, the faster the virus gets diluted. Everyday face coverings reduce the amount of virus projected, but aren’t total blockades.
Loud talking, heavy breathing, singing, and screaming expel more virus, which is why experts point to nightclubs and gyms as risky businesses to be open. (That’s not to say it’s impossible to catch the virus while having a quiet conversation with someone outside — it’s just less likely.)
The reason having prolonged, proximate contact with someone is riskier is in part because there is a threshold level of virus you need to be exposed to to become infected. (More on this later.) Also, one hypothesis for why some people get so sick is that they are exposed to higher “doses” of virus.
Researchers are also finding that some relatively small proportion of infected people — maybe 10% to 20% — are driving some 80% of new cases, often through “superspreading” events in indoor settings like bars, meat processing plants, and homes.
Whether such transmission occurs depends on a host of variables: how many people are in a given place, what the ventilation in the room is like, and, of course, whether someone with infectious C19 is there. Some people might shed more virus than others, and people are more or less likely to spread the virus during different points in their infection. Evidence suggests that contagiousness spikes in the days before people who will go on to show symptoms start feeling sick.

People can test positive for a long time after they recover. It doesn’t matter

There was a lot of angst a few months ago about some people who had seemingly recovered from C19 infections continuing to test positive for the virus for weeks. Were they infectious? Should recommendations be changed for how long infected people should be isolated?
It turns out it is an issue of testing. Most testing is conducted using a platform called PCR — polymerase chain reaction — that looks for tiny fragments of the coronavirus. But the test can’t tell if those sections of genetic code are part of actual viruses that can infect someone else, or fragments of viruses that are absolutely no threat.
It’s clear now that people who had mild or uncomplicated infections shed active virus for somewhere up to 10 days after their symptoms started. (“Severely ill or immunocompromised patients do shed infectious virus for longer,” said Malik Peiris, a coronavirus expert at Hong Kong University.)
The weeks and weeks of positive tests — like those that prevented this woman in Quebec from cuddling her infant son for 55 days — don’t tell us that these people are still a risk to others. “In fact, we know that they are not infectious for that long,” said Maria Van Kerkhove, the World Health Organization’s leading coronavirus expert.

After the storm, there are often lingering effects

Name a body part or system and C19 has left its fingerprints there. We know this: Unusually sticky blood can clog vessels on the way to the heart and inside the brain and lungs of infected people, causing heart attacks, strokes, and deadly pulmonary embolisms. There are growing worries that these and other health effects will be long-lasting.
Heart: The hyperinflammation of an immune response triggered by the virus can weaken heart muscles so much that even young people who had mild infections may be at risk for future heart failure, cardiac MRIs in Germany indicate. More immediately, some people have chest pain or feel like their hearts are racing as they recover from the infection. And college athletes are no exception
Brain: People whose first C19 symptom might have been losing their sense of smell and taste may find their anosmia persists. Headaches and dizziness are common. Mood disorders such as anxiety, depression, and PTSD follow in the wake of infection, and the mental confusion called “Covid fog” leaves people searching for words, struggling with simple math, or simply trying to think.
Peripheral nervous system: In Italy, 3 C19 patients experienced myasthenia gravis, an autoimmune disorder, possibly due to demyelination. Demyelination, in which the protective coating of nerve cells is attacked by the immune system, can cause weakness, numbness, and tingling. In some cases it can spur psychosis and hallucinations. Some patients have Guillain-Barre syndrome, a rare autoimmune disease that interferes with nerve signals, leading to abnormal sensations, weakness, and sometimes paralysis.

‘Long-haulers’ don’t feel like they’ve recovered

They have a name, a growing social media presence, and a problem. They are the “long-haulers,” people who have survived their C19 infections but feel a long way from normal. We know they’re out there, but we don’t know how many, why their symptoms persist, and what happens next.
In July, a survey conducted by the CDC found that 35% of people who tested positive for the coronavirus and had symptoms of C19 — cough, fatigue, or shortness of breath — but were not hospitalized had not returned to their previous health two to three weeks later. Among those between 18 and 34 years old who had no previous chronic conditions, 20% felt prolonged signs of illness.
The National Heart, Lung, and Blood Institute has launched an observational study to track the long-term effects of C19, aiming to follow 3,000 patients 6 months after being discharged from 50 hospitals.
Mount Sinai Health System in New York City opened a Center for Post-Covid Care in May to treat long-haulers. David Putrino, director of rehabilitation innovation there, has suggested dysautonomia — when heart rate, blood pressure, and body temperature are disjointed —could be to blame for prolonged and distressing symptoms. Why C19 would cause this isn’t known, nor is the best treatment.

Vaccine development can be accelerated. A lot

The world still doesn’t have a vaccine that has been shown to be protective against C19, though China and Russia have issued emergency use licenses for partially tested vaccines.
But an extraordinary amount of progress toward C19 vaccines has been made, in record time. Trials have been compressed and overlapped, with manufacturers running Phase 1/2 trials in some cases and Phase 2/3 trials in others.
Meanwhile, they’ve been building out production capacity to be able to produce hundreds of millions of doses and have started production, even before finding out whether their vaccine candidate actually works. This work is being done with substantial financial support of governments, the Bill and Melinda Gates Foundation, and CEPI, the Coalition for Epidemic Preparedness Innovations.
It’s called “at risk” production — and the term is apt. If some of these vaccines don’t work, that output will have to be junked. But if Phase 3 trials show they do work, deployment could begin as soon as the FDA, or a regulator in another country, approves any of these vaccines.
That means vaccination with fully approved vaccines could begin as soon as about a year after the discovery of the new virus. This constitutes a revolution in vaccine development.

People without symptoms can spread the virus

Discussing asymptomatic cases of C19 automatically raises some headache-inducing semantic issues. Some people are truly asymptomatic throughout their infections, but the word is often also used to describe people who are presymptomatic — those who will show symptoms but haven’t yet. Other people don’t show classic C19 symptoms — fever, cough, loss of smell — but just feel kinda crappy for a day. Where do they fit in?
Whatever group you’re talking about, there are some key implications for the pandemic, and trying to rein it in. One: Some%age of infected people — roughly 20%, according to one recent review, though other studies have produced higher estimates — do not show symptoms at all. And two: Whether or not someone is asymptomatic or presymptomatic, they can still spread the virus (though whether they spread it as efficiently as people with symptoms is still unknown). That is why public health campaigns have been stressing distancing, masks, and hand hygiene for everyone, not just people who feel sick. Once you do start showing symptoms and try to restrict contact with others, it is too late to prevent spread.

Mutations to the virus haven’t been consequential

Coronaviruses in general do not mutate very quickly compared to other viral families. This is a good thing: The leading vaccine candidates, for example, are based on the coronavirus’ genetic sequence, so theoretically a major change in that lineup could hinder the effectiveness of any vaccine. So far, that doesn’t seem to have happened.
Still, scientists have noticed smaller changes in the genome. The one that has gotten the most attention was one swap in the “letters” that make up the virus’ RNA, which created the “G variant.” The switch happened early in the pandemic, and the G variant has since become dominant around the world. Scientists haven’t been able to figure out, however, whether the G variant is outcompeting its predecessor — perhaps it’s more contagious? — or if that’s just chance.
And so far, they haven’t landed on evidence that people who contract the G variant get more or less sick than those infected by the other variant. It could just be a mutation that’s like changing your T-shirt from navy blue to royal blue — an aesthetic difference, but something pretty neutral.

Viruses on surfaces probably aren’t the major transmission route

Throughout the spring, you could barely find hand sanitizer. Fears that viruses lurking on surfaces could infect us with C19 turned most of us into zealous surface cleaners. Some people went so far as to quarantine their mail, not touching it for days as they waited for potential lingering viruses to die.
The general consensus now is that “fomites” — germs on surfaces — aren’t the major transmission route for C19. Van Kerkhove of WHO said there hasn’t been a case recorded where it’s clear someone was infected by fomites alone.
(In the real world, someone in close enough contact with an infected person to become infected will likely have encountered viruses on surfaces and virus-laced droplets and maybe even small, aerosol-sized particles containing the virus that have been expelled by coughing, singing, or speaking. Teasing out of that situation which route of transmission triggered infection may be impossible to do.)
But it’s clear from lots of studies that surfaces around infected people can be contaminated with viruses and the viruses can linger. Cleaning surfaces and being prudent about hand hygiene is a risk-lowering step people can take, public health officials agree.

What We Don’t Know

People seem to be protected from reinfection, but for how long?

The thinking is that a case of C19, like other infections, will confer some immunity against reinfection for some amount of time. But researchers won’t know exactly how long that protection lasts until people start getting C19 again.
So far, despite some anecdotal reports, scientists have not confirmed any repeat C19 cases.
All that supports the notion that C19 acts like other viral infections, including illnesses caused by other coronaviruses. Researchers are finding that most infected people mount an immune response involving both antibodies and immune cells that clears the virus, and that persists for some amount of time. Reports of waning antibody levels incited some concern that perhaps protection to the coronavirus might not last very long, with big implications for the frequency of required vaccine boosts. But immunologists have pointed out that antibodies for other viruses wane as well; their levels surge upon re-exposure to the pathogen and they can still halt reinfection.
Researchers don’t know for sure what level of antibodies are required to block the virus from gaining a toehold in cells, and what role pathogen-fighting T cells might have in fending off an infection. People who recover from C19 also produce varying levels of antibodies — it’s possible people who generate a weaker initial immune response might not be protected for as long from reinfection.
“We don’t know for how long that immune response lasts,” the WHO’s Van Kerkhove said last week. “We don’t know how strong it is.”

What happens if or when people start having subsequent infections?

Given that most respiratory viruses are not “one-and-done” infections — they don’t induce life-long immunity in the way a virus like measles does — there is a reasonable chance that people could have more than one infection with C19.
Experience with human coronaviruses — which mostly cause colds — supports that idea. A study in the Netherlands followed people for decades, measuring their antibodies to four human coronaviruses at regular intervals and looking for changes that would indicate a new infection. The scientists found that reinfection could occur within a year of the first infection. (The study is a preprint, meaning it hasn’t yet been through the peer review process.)
Some scientists have theorized that on subsequent infections, immune systems might mount quicker responses to C19, leading to milder infections. If that’s true, the coronavirus virus might transition into a less daunting threat over time. But it’s still a big unknown. “We don’t know,” Van Kerkhove said. “I don’t want to speculate.”

How much virus does it take to get infected?

Whether you become infected or not when you encounter a pathogen isn’t just a question of whether you’re susceptible or immune. It depends on how much of the virus (or bacterium) you encounter.
And the amount capable of tipping the balance is what’s known as the minimum infectious dose. Some pathogens have a low infectious dose. For example, it doesn’t take a lot of E. coli 0157, a dangerous bacterium transmitted in food, to make someone sick.
How big a dose of the coronavirus does it take to infect most people? It’s one of the burning questions in coronavirus research, said Angela Rasmussen, a coronavirus expert at Columbia University. “We don’t know the amount that is required to cause an infection, but it seems that it’s probably not a really, really small amount, like measles.”

How many people have been infected?

There have been 21 million confirmed cases of C19 around the world, and 5.3 million in the United States. Far more people than that have actually had the virus.
Problems with testing, and its limited availability, have contributed to that gap, as has the fact that some people have such mild or no symptoms that they don’t know they’re infected. But researchers don’t know just how big of a gulf they’re dealing with — how much spread they’ve missed.
“Serosurveys” — which rely on testing for the level of the coronavirus antibodies in a community — are starting to help fill in some knowledge. A recent CDC study of 10 cities and states estimated that in most places, the true number of infections was some 10 times higher than the number of confirmed cases.
Still, that leaves perhaps 20% of people, even in hard-hit communities, with potential immunity to C19. That means that herd immunity — the point at which so many people are immune that the virus can’t circulate — remains far off even in areas that have suffered severe outbreaks.

It’s not clear why some people get really sick, and some don’t

The sheer range of outcomes for people who get C19 — from a truly asymptomatic case, to mild symptoms, to moderate disease leading to months-long complications, to death — has befuddled infectious disease researchers.
There are some clear factors for who faces higher risks of getting severely ill: older people, as well as people with conditions ranging from cancer to obesity to sickle cell disease.
But scientists have postulated that a host of other underlying factors could help dictate why most healthy 30-year-olds shake off the virus after a couple days and some get severely ill. Researchers are studying genetic differences in patients, while others are looking at blood type.
Recent studies have pointed to another potential player. Perhaps up to half the population has immune-system T cells that were initially generated in response to an infection by one of the common cold-causing coronaviruses but that can recognize the coronavirus as well. These “cross-reactive” T cells could help give the immune system the boost it needs to stave off serious symptoms, but researchers don’t know for sure what role, if any, they actually play.

Source: Seven months later, what we know — and don’t know — about Covid-19

2. What if ‘Herd Immunity’ Is Closer Than Scientists Thought?

We’ve known from the beginning how the end will arrive. Eventually, the coronavirus will be unable to find enough susceptible hosts to survive, fading out wherever it briefly emerges.
To achieve so-called herd immunity — the point at which the virus can no longer spread widely because there are not enough vulnerable humans — scientists have suggested that perhaps 70% of a given population must be immune, through vaccination or because they survived the infection.
Now some researchers are wrestling with a hopeful possibility. In interviews with The New York Times, more than a dozen scientists said that the threshold is likely to be much lower: just 50%, perhaps even less. If that’s true, then it may be possible to turn back the coronavirus more quickly than once thought.
The new estimates result from complicated statistical modeling of the pandemic, and the models have all taken divergent approaches, yielding inconsistent estimates. It is not certain that any community in the world has enough residents now immune to the virus to resist a second wave.
But in parts of New York, London and Mumbai, for example, it is not inconceivable that there is already substantial immunity to the coronavirus, scientists said.
“I’m quite prepared to believe that there are pockets in New York City and London which have substantial immunity,” said Bill Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health. “What happens this winter will reflect that.”
“The question of what it means for the population as a whole, however, is much more fraught,” he added.
Herd immunity is calculated from the epidemic’s so-called reproductive number, R₀, an indicator of how many people each infected person spreads the virus to.
The initial calculations for the herd immunity threshold assumed that each community member had the same susceptibility to the virus and mixed randomly with everyone else in the community.
“That doesn’t happen in real life,” said Dr. Saad Omer, director of the Yale Institute for Global Health. “Herd immunity could vary from group to group, and subpopulation to subpopulation,” and even by postal codes, he said.
For example, a neighborhood of older people may have little contact with others but succumb to the virus quickly when they encounter it, whereas teenagers may bequeath the virus to dozens of contacts and yet stay healthy themselves. The virus moves slowly in suburban and rural areas, where people live far apart, but zips through cities and households thick with people.
Once such real-world variations in density and demographics are accounted for, the estimates for herd immunity fall. Some researchers even suggested the figure may be in the range of 10 to 20%, but they were in the minority.
Assuming the virus ferrets out the most outgoing and most susceptible in the first wave, immunity following a wave of infection is distributed more efficiently than with a vaccination campaign that seeks to protect everyone, said Tom Britton, a mathematician at Stockholm University.
His model puts the threshold for herd immunity at 43% — that is, the virus cannot hang on in a community after that%age of residents has been infected and recovered.
Still, that means many residents of the community will have been sickened or have died, a high price to pay for herd immunity. And experts like Dr. Hanage cautioned that even a community that may have reached herd immunity cannot afford to be complacent.
The virus may still flare up here and there, even if its overall spread is stymied. It’s also unclear how long someone who has recovered may be immune, and for how long.

Virus-Resistant Communities?

The coronavirus crashed this year’s Purim celebrations in the Orthodox Jewish neighborhoods of New York City, tearing through the parades and masquerades in Brooklyn on March 9 and 10.
Schools and synagogues soon shut down to quell the spread, but it was too late. By April, thousands in the Brooklyn communities were infected, and hundreds had died.
“It’s like a black hole in my memory because of how traumatic it was,” said Blimi Marcus, a nurse practitioner who lives in Borough Park, which was hit hard by the virus.
But all that has changed now, Ms. Marcus added: “The general feeling is one of complacency, that somehow we’ve all had it and we’re safe.”
Is it possible that some of these communities have herd immunity? In some clinics, up to 80% of people tested had antibodies to the virus. The highest prevalence was found among teenage boys.
But people at clinics are more likely to be showing symptoms and therefore more likely to be infected, said Wan Yang, an epidemiologist at Columbia University’s Mailman School of Public Health in New York. Random household surveys would probably find lower rates — but still well above the 21% average reported for New York City, she said.
Researchers in Mumbai conducted just such a random household survey, knocking on every fourth door — or, if it was locked, the fifth — and took blood for antibody testing. They found a startling disparity between the city’s poorest neighborhoods and its more affluent enclaves. Between 51 and 58% of residents in poor areas had antibodies, versus 11 to 17% elsewhere in the city.
The lowest-income residents are packed tightly together, share toilets, and have little access to masks. “These factors contributed to a silent infection spread,” said Dr. Jayanthi Shastri, a microbiologist at Kasturba Hospital in Mumbai who led the work.
Most researchers are wary of concluding that the hardest-hit neighborhoods of Brooklyn, or even those in blighted areas of Mumbai, have reached herd immunity or will be spared future outbreaks.
But models like Dr. Britton’s hint that it’s not impossible. Other researchers have suggested, controversially, that herd immunity can be achieved at rates of immunity as low as 10 or 20% — and that entire countries may already have achieved that goal.
Criticism trailed Sunetra Gupta, a theoretical epidemiologist at Oxford University, after a widely circulated interview in which she said that London and New York may already have reached herd immunity because of variability among people, combined with a theoretical immunity to common cold coronaviruses that may protect against the new one.
“That could be the explanation for why you don’t see a resurgence in places like New York,” she said.
Most experts reject that notion. Several studies have shown that certain immune cells produced following infection with seasonal coronaviruses may also recognize the new coronavirus.
But “where is the evidence that it’s protective?” asked Natalie Dean, a biostatistician at the University of Florida.
These cities have not returned to pre-pandemic levels of activity, other experts noted.
“We are still nowhere near back to normal in our daily behavior,” said Virginia Pitzer, a mathematical epidemiologist at the Yale School of Public Health. “To think that we can just stop doing all that and go back to normal and not see a rise in cases I think is wrong, is incorrect.”
A second wave might also hit groups or neighborhoods that were spared by the first, and still wreak havoc, she said. Immunity is a patchwork quilt in New York, for instance: Antibodies were present in 68% of people visiting a clinic in the Corona neighborhood of Queens, for instance, but in just 13% of those tested at a clinic in the Cobble Hill section of Brooklyn.
But another group, led by the mathematician Gabriela Gomes of the University of Strathclyde in Britain, accounted for variations within a society in its model and found that Belgium, England, Portugal and Spain have herd immunity thresholds in the range of 10 to 20%.
“At least in countries we applied it to, we could never get any signal that herd immunity thresholds are higher,” Dr. Gomes said. “I think it’s good to have this horizon that it may be just a few more months of pandemic.”
Other experts urged caution, saying these models are flawed, as all models are, and that they oversimplify conditions on the ground.
Jeffrey Shaman, an epidemiologist at Columbia University, said it wasn’t clear to him that Dr. Gomes’s model offered only one possible solution. And he was suspicious of the big ranges among the four countries.
“I think we’d be playing with fire if we pretended we’re done with this,” Dr. Shaman said.
The new models offer food for thought, he and other experts said, but should not be used to set policy.
“Mathematically, it’s certainly possible to have herd immunity at these very, very low levels,” said Carl Bergstrom, an infectious disease expert at the University of Washington in Seattle. “Those are just our best guesses for what the numbers should look like.”
“But,” he added, “they’re just exactly that, guesses.”

Imperfect Immunity

But what about immunity at levels lower than those needed for herd immunity?
“Definitely the disease would not spread as well if it gets back into New York,” said Joel Miller, a mathematical modeler at La Trobe University in Australia. “The same level of behavior change will have more effect on the disease now than it did four months ago.”
Thinking of a city or country as composed of subgroups, demarcated by age, race and level of social activity, might also help governments protect those with the least immunity.
That perspective also might help put a renewed focus on groups who require the higher levels of immunity, because of greater exposure levels and other inequities, including Black and Latino residents, said Dr. Manoj Jain, an infectious disease expert at Emory University. “That’s where this info is very useful,” he said.
The models also suggest a vaccination strategy: Rather than uniformly vaccinate all groups, governments could identify and immunize those most likely to be exposed in “superspreader” events.
“Getting those people vaccinated first can lead to the greatest benefit,” said Dr. Michael Mina, an immunologist at Harvard University. “That alone could lead to herd immunity.”
Vaccination schemes for other pathogens have successfully exploited this approach. For example, when children were given the pneumococcal vaccine in the early 2000s, rates of bacterial pneumonia in the elderly rapidly dropped because of a “herd effect.”
Vaccines that offer just 50% protection are considered to be moderately effective, but at that efficiency, even a low herd immunity target would require that a large proportion of the population be immunized, Dr. Bergstrom noted.
If there are early reports of side effects that may scare away some people, he said, “we’d do well to start thinking about all that now.”
Back in Brooklyn, fewer than 1% of people tested at neighborhood clinics over the past 8 weeks were infected with the virus. But there are still handfuls of cases, Ms. Marcus said, adding that her 10-year-old niece was in quarantine because a counselor at her day camp had tested positive.
“Sometimes that’s all you need, right?” she said. “I’m still hoping we don’t see what we had in March and April, but I’m not so sure that we’ve seen the end of it.”

Source: What if ‘Herd Immunity’ Is Closer Than Scientists Thought?

D. New Scientific Findings & Research

1. Mild C19 cases can produce strong T cell response

Mild cases of C19 can trigger robust memory T cell responses, even in the absence of detectable virus-specific antibody responses, researchers report August 14 in the journal Cell. The authors say that memory T cell responses generated by natural exposure to or infection with the coronavirus may be a significant immune component to prevent recurrent episodes of severe disease.
“We are currently facing the biggest global health emergency in decades,” says senior author Marcus Buggert (@marcus_buggert) of the Karolinska Institutet. “In the absence of a protective vaccine, it is critical to determine if exposed or infected people, especially those with asymptomatic or very mild forms of the disease who likely act inadvertently as the major transmitters, develop robust adaptive immune responses against the coronavirus.”
To date, there is limited evidence of reinfection in humans with previously documented C19. Most studies of immune protection against the coronavirus in humans have focused on the induction of neutralizing antibodies. But antibody responses tend to wane and are not detectable in all patients, especially those with less severe forms of C19. Research in mice has shown that vaccine-induced memory T cell responses, which can persist for many years, protect against the coronavirus, even in the absence of detectable antibodies. Until now, it was not clear how coronavirus T cell responses relate to antibody responses or to the clinical course of C19 in humans.
To address this gap in knowledge, Buggert and his collaborators assessed coronavirus specific T cell and antibody responses in more than 200 individuals from Sweden across the full spectrum of exposure, infection, and disease. During the acute phase of infection, the T cell responses were associated with various clinical markers of disease severity. After recovery from C19, coronavirus specific memory T cell responses were detectable. The strongest T cell responses were present in individuals who recovered from severe C19. Meanwhile, progressively lower T cell responses were observed in individuals who recovered from very mild C19, and family members exposed to the virus.
In line with expectations, all 23 individuals who recovered from severe C19 developed both coronavirus-specific antibody and T cell responses. But surprisingly, coronavirus-specific memory T cell responses were detected months after infection in exposed family members and in most individuals with a history of very mild C19, sometimes in the absence of SARS-CoV-2-specific antibodies. Among the 28 exposed family members, only 17 (a few more than half) had detectable antibody responses, whereas nearly all (26/28) showed T cell responses. Among the 31 individuals who recovered from mild C19, almost all had detectable antibody responses (27/31) and developed T cell responses (30/31).
“Our findings suggest that the reliance on antibody responses may underestimate the extent of population-level immunity against the coronavirus,” Buggert says. “The obvious next step is to determine whether robust memory T cell responses in the absence of detectable antibodies can protect against C19 in the long-term.”

Source: Mild COVID-19 cases can produce strong T cell response

2. Acupuncture could help coronavirus patients

As the world waits on pins and needles for a vaccine, acupuncture could offer relief to those suffering from the coronavirus.
A new study out of Harvard Medical School found that acupuncture can help ease inflammation in mice.
The traditional Chinese practice influenced rodents’ ability to cope with a cytokine storm — an overly aggressive immune response which has been found to lead to lung inflammation, pneumonia and death in some C19 patients, according to the study published Wednesday in the journal Neuron.
A number of drugs are currently being tested to try and quell the sometimes lethal reaction, but the Harvard researchers say this classic Chinese medical practice may be the answer.
“This is exciting news,” acupuncturist Sara Reznikoff, who was not affiliated with the study, told The Post. “It’s always nice when Western studies back up the ancient healing medical system of acupuncture and traditional Chinese medicine.”
The findings, however, don’t surprise her.
“Acupuncture is fantastic at triggering the body’s innate healing abilities, helping with inflammation and calming the nervous system. I have seen great results at my practice, treating patients with post-C19 symptoms,” said Reznikoff, who runs her own practice in Brooklyn. “I’m glad that acupuncture is being considered in the fight against C19 — anything that helps.”
While the findings are relevant now, they could have implications long after the world recovers from the pandemic, the researchers said.
Cytokine storms have “gained mainstream attention as a complication of severe C19, but this aberrant immune reaction can occur in the setting of any infection and has been long known to physicians as a hallmark of sepsis, an organ-damaging, often-fatal inflammatory response to infection” a press release for the study explained.
Another study described the response as such: “The term ‘cytokine storm’ calls up vivid images of an immune system gone awry and an inflammatory response flaring out of control.”
In the new study, researchers found that mice experiencing a cytokine storm had a 40% greater chance of survival when treated with electroacupuncture.
As well, acupuncture worked well as a preventative practice: Mice treated with acupuncture before developing a cytokine storm experienced lower levels of inflammation and their survival rate increased from 20 to 80%.

Source: How acupuncture could help coronavirus patients, study says

E. Improved & Potential Treatments

1. NIH Launches ACTIV-3 Clinical Trial to Test Antibody Treatments in Hospitalized C19 Patients

Patients admitted with C19 at select hospitals may now volunteer to enroll in a clinical trial to test the safety and efficacy of a potential new treatment for the disease. The Phase 3 randomized, controlled trial is known as ACTIV-3, and as a “master protocol,” it is designed to expand to test multiple different kinds of monoclonal antibody treatments. It also can enroll additional volunteers in the middle of the trial, if a specific investigational treatment shows promise.
The new study is one of four ongoing or planned trials in the National Institutes of Health. Accelerating C19 Therapeutic Interventions and Vaccines (ACTIV) program, a public-private partnership to speed development of the most promising treatments and vaccine candidates. It also is receiving support through Operation Warp Speed, the U.S. government’s multi-agency effort to develop, manufacture and distribute medical countermeasures to fight C19.
The trial will take place at select hospitals around the world that are part of existing clinical trial networks. They include the lead network, the International Network of Strategic Initiatives in Global HIV Trials (INSIGHT), operated by the National Institute of Allergy and Infectious Diseases (NIAID), a part of the National Institutes of Health. Collaborating clinical trial networks include the Prevention and Early Treatment of Acute Lung Injury network (PETAL) and Cardiothoracic Surgical Trials Network (CTSN), supported by the NIH’s National Heart, Lung and Blood Institute through the Collaborating Network of Networks for Evaluating C19 and Therapeutic Strategies (CONNECTS) program, and the U.S. Department of Veterans Affairs Medical Centers.
“Under Operation Warp Speed, the U.S. Government has brought together multiple agencies to accelerate the development, manufacture and distribution of medical countermeasures for C19,” said NIH Director Dr. Francis S. Collins, M.D., Ph.D. “The ACTIV studies are just a few examples of this critical activity, which emphasizes flexibility and minimizes delays to generate scientifically sound results.”
ACTIV-3 uses an adaptive two-stage Phase 3 protocol design. The ACTIV-3 trial can be modified to test additional experimental therapeutics and flexibly allow novel therapeutics to enter at either stage 1 or stage 2. In addition, if a treatment appears to be safe and effective in the initial stage after review by an independent data and safety monitoring board (DSMB), the investigational therapeutic proceeds to stage 2 testing, where more volunteers are enrolled. If an investigational therapeutic is unsafe or not likely to be effective, it will be dropped.
The ACTIV-3 study will begin by studying the investigational monoclonal antibody LY-CoV555, which was identified in a blood sample from a recovered C19 patient. Antibodies are infection-fighting proteins made by the immune system that can bind to the surface of viruses and prevent them from infecting cells. Synthetic versions of antibodies can be reproduced in a laboratory. These manufactured antibodies are known as monoclonal antibodies. The LY-CoV555 antibody was discovered by Abcellera Biologics (Vancouver, British Columbia) in collaboration with NIAID’s Vaccine Research Center. Subsequently, it was developed and manufactured by Lilly Research Laboratories, Eli Lilly and Company (Indianapolis, Indiana), in partnership with AbCellera. The investigational product also is being tested in another ongoing NIAID study, ACTIV-2, which is studying its safety and efficacy in people with mild to moderate symptoms of C19 who have not been hospitalized. Safety data and other findings will be shared across the ACTIV-2 and ACTIV-3 studies through the DSMB.
“Studying the impact of this investigational therapeutic on multiple patient populations at the same time is critical to determining whether it can help C19 patients with differing levels of disease severity,” said NIAID Director Anthony S. Fauci, M.D. “These concurrent trials have the potential to yield significant and comprehensive clinical data.”
The initial stage of the ACTIV-3 clinical trial aims to enroll approximately 300 volunteers who have been hospitalized with mild to moderate C19 with fewer than 13 days of symptoms. Once their C19 infections have been confirmed and they have consented to take part in the study, participants will be randomly assigned to receive either an intravenous (IV) infusion of LY-CoV555 or a saline placebo infusion. Participants also will receive standard care for C19, including the antiviral remdesivir. After five days, participants’ symptoms will be assessed, as will their need for supplemental oxygen, mechanical ventilation, or other supportive care. Volunteers will be followed for 90 days after enrollment and will receive regular examinations and have blood samples taken periodically during this time to analyze their response to the investivational therapeutic.
Data collected on the fifth day of the volunteers’ participation will determine whether the investigational therapeutic will be administered to a larger group of volunteers. If LY-CoV555 appears to be safe and appears to be effective, the trial will enroll an additional 700 participants. It also will begin enrolling more severely ill participants, such as those with organ failure requiring mechanical support, or C19-associated dysfunction of organs other than the lungs. The primary endpoint of the trial is the participants’ sustained recovery for 14 days after release from the hospital.
The principal investigator of ACTIV-3 is Jens Lundgren, M.D., of the University of Copenhagen and Rigshospitalet. Leads of the participating networks include James Neaton, Ph.D., of the INSIGHT network, Taylor Thompson, M.D., of the PETAL network, Annetine Gelijns, Ph.D., and Alan Moskowitz, M.D., of the CTSN, and Rachel Ramoni, D.M.D., Sc.D., of the U.S. Department of Veterans Affairs. To ensure that the trial is being conducted in a safe and effective manner, an independent DSMB will oversee the trial and conduct periodic reviews of the accumulating data.

Source: NIH Launches ACTIV-3 Clinical Trial to Test Antibody Treatments in Hospitalized COVID-19 Patients

2. C19 Treatment Possible As Preexisting Drug Shows Promise in Fight Against the Coronavirus

A team of researchers at the Pritzker School of Molecular Engineering (PME) at the University of Chicago used state-of-the-art computer simulations to identify a preexisting drug that could fast-track a solution to this worldwide pandemic.
Early in February, concerned by the rapid progress of the pandemic, Professor Juan de Pablo and his students used their molecular modeling expertise to help find a treatment against the disease. They were not the only ones. Other groups around the world were beginning to use supercomputers to rapidly screen thousands of existing compounds for potential use against the coronavirus.
“By virtue of the large number of compounds considered in high throughput screens, those calculations must necessarily involve a number of simplifications, and the results must then be evaluated using experiments and more refined calculations,” de Pablo explained.
Researchers first focused on finding a weakness in the virus to target. They chose its main protease: Mpro. Mpro is a key coronavirus enzyme that plays a central role in the virus’ life cycle. It facilitates the virus’ ability to transcribe its RNA and replicate its genome within the host cell.
A pharmaceutical drug that shows promise as a weapon against Mpro is Ebselen. Ebselen is a chemical compound with anti-viral, anti-inflammatory, anti-oxidative, bactericidal, and cell-protective properties. Ebselen is used to treat multiple diseases, including bipolar disorders and hearing loss. In combination with silver, Ebselen treats five clinically difficult-to-manage antibiotic-resistant Gram-negative bacteria. Several clinical trials have proven its safety for use in humans.

How It Works

Professor Juan de Pablo and his students set out to develop detailed models of the enzyme and the drug. Using those models and sophisticated supercomputer simulations, they discovered that the small Ebselen molecule is able to decrease Mpro’s activity in two different ways.
“In addition to binding at the catalytic site of the enzyme, Ebselen also binds strongly to a distant site, which interferes with the enzyme’s catalytic function by relying on a mechanism in which information is carried from one region of a large molecule to another region far away from it through subtle structural reorganizations,” de Pablo says.
That finding was particularly important because it helped explain Ebselen’s potential efficacy as a repurposed drug, and it revealed a new vulnerability in the virus that was previously not known and that could be use useful in developing new therapeutic strategies against C19.
By working around the clock, the team completed their work in just over two months and submitted their manuscript to public research archives in April for others to consider.

Drug Development Potential

The research team’s discovery of two binding sites looks promising for Ebselen to be a new drug lead for the design and development of new Mpro inhibitors and C19 treatment. Motivated by their findings, de Pablo and his student are quick to point out that much work is yet to be done.
“The main protease is one of many proteins in the virus that could be targeted with existing, repurposed drugs, and there are thousands of compounds to be considered,” de Pablo says. “We are systematically investigating each of the proteins involved in the virus function and investigating their vulnerabilities and their responses to a wide range of drugs.”
de Pablo and his team will soon release a comprehensive study of the RBD/ACE2 complex from the virus and another drug that offers promise to interfere with the binding of the virus to cells.

Source: COVID-19 Treatment Possible As Preexisting Drug Shows Promise in Fight Against the SARS-CoV-2 Virus

F. Testing & Masks

1. FDA clears saliva test for C19, opening door to wider testing

The FDA on Saturday authorized emergency use of a new and inexpensive saliva test for C19 that could greatly expand testing capacity.
The new test, which is called SalivaDirect and was developed by researchers at the Yale School of Public Health, allows saliva samples to be collected in any sterile container. It is a much less invasive process than the nasal swabs currently used to test for the virus that causes C19, but one that has so far yielded highly sensitive and similar results. The test, which also avoids a key step that has caused shortages of chemical reagents used in other tests, can run approximately 90 samples in fewer than three hours in a lab, although the number can be greater in big labs with automation.
Moreover, Yale intends to provide its “open source” testing protocol to laboratories around the country. Other labs can now adopt the method while using a variety of commercially available testing components that can reduce costs, speed turnaround times and increase testing frequency, according to the FDA. And because the reagents for the test cost less than $5, the Yale researchers estimated labs should charge about $10 per sample, although that remains to be seen. The testing method is available immediately, but the researchers added it can be scaled up quickly for use in the coming weeks.
“Providing this type of flexibility for processing saliva samples to test for C19 infection is groundbreaking in terms of efficiency and avoiding shortages of crucial test components like reagents,” said FDA Commissioner Stephen Hahn in a statement. The agency has previously authorized four other tests that use saliva for sampling, but these yielded varying results.
The authorization occurs amid ongoing disarray over C19 testing. The U.S. has been plagued by an inconsistent strategy for detecting the virus, thanks in part to persistent shortages and the use of a variety of different tests that have sometimes yielded unreliable results.
The inability to quickly and efficiently test Americans has, in turn, made it much harder for government officials and the medical community to accurately assess and predict the path of the virus. For this reason, the FDA move was greeted with enthusiasm by some public health experts, who have bemoaned the ongoing spread of C19.
“This could be one the first major game changers in fighting the pandemic,” tweeted Andy Slavitt, a former acting administrator of the Centers for Medicare and Medicaid Services in the Obama administration, who expects testing capacity to be expanded significantly. “Rarely am I this enthusiastic… They are turning testing from a bespoke suit to a low-cost commodity.”
Yale’s saliva-based test also skirts a step that other C19 tests require: extracting the virus’s genetic material. Extraction kits are one of many components of the existing diagnostic tests that have faced shortages. Supply issues have limited testing capacity overall, as well as slowed how quickly results can be returned.
“Widespread testing is critical for our control efforts,” Yale researcher Nathan Grubaugh said in a statement. Grubaugh added: “If cheap alternatives like SalivaDirect can be implemented across the country, we may finally get a handle on this pandemic, even before a vaccine.”
The research team validated SalivaDirect in part by testing NBA players, coaches, and staff, and Yale said the test is now being studied in asymptomatic people through the program with the NBA and its players union.

Source: FDA Clears Saliva Test

2. New C19 Virus-Filtering Mask Material Being Fast-Tracked to Market

A new company, CelluAir, will bring the world-first, virus-filtering mask material made from agriculture waste to market. The material was developed by QUT process engineer Dr. Thomas Rainey and his research team.
The material, which can filter nanoparticles smaller than the coronavirus, will be fast-tracked into production after proof of concept testing found it could filter nanoparticles smaller than 100 nanometers, the size of a virus, while retaining high breathability which reduces wearer fatigue.
CelluAir, a start-up managed by Australian commercialization company Innovyz, signed a license agreement and a shareholders’ agreement with QUT on Friday. CelluAir will begin an accelerated six-week scope of work to scale up the technology to bring it to market as soon as possible.
CelluAir will be a joint venture between QUT and Innovyz.
Innovyz is known for having incubated many advanced manufacturing start-ups from research including listing Amaero (3DA) from Monash University, and Titomic (TTT) from CSIRO on the Australian Stock Exchange in 2019 and 2017 respectively.
“The new material is relatively cheap to produce and is biodegradable making it sustainable for single use,” Dr. Rainey, from QUT Science and Engineering Faculty’s School of Mechanical, Medical and Process Engineering, said.
“Our tests showed the new material was more breathable than commercial face masks, including surgical masks. Breathability is the pressure or effort the wearer has to use to breathe through the mask.
“The higher the breathability the greater the comfort and reduction in fatigue. This is an important factor for people who have to wear masks for long periods or those with existing respiratory conditions.”
Innovyz general manager Tom Kenyon said the company specialized in taking research from the laboratory and moving to market.
“We’re super excited to be working with QUT which has a great reputation in research and are very focused on commercial outcomes. Many researchers want their research to have impact and the quickest way to have impact is to bring that research to market.”

Source: New COVID-19 Virus-Filtering Mask Material Being Fast-Tracked to Market

3. Titanate Nanowire Mask Filter Can Kill Coronavirus

As part of attempts to curtail the C19 pandemic, paper masks are increasingly being made mandatory. Their relative effectiveness is no longer in question, but their widespread use has a number of drawbacks. These include the environmental impact of disposable masks made from layers of non-woven polypropylene plastic microfibres. Moreover, they merely trap pathogens instead of destroying them. “In a hospital setting, these masks are placed in special bins and handled appropriately,” says László Forró, head of EPFL’s Laboratory of Physics of Complex Matter. “However, their use in the wider world – where they are tossed into open waste bins and even left on the street – can turn them into new sources of contamination.”
Researchers in Forró’s lab are working on a promising solution to this problem: a membrane made of titanium oxide nanowires, similar in appearance to filter paper but with antibacterial and antiviral properties.
Their material works by using the photocatalytic properties of titanium dioxide. When exposed to ultraviolet radiation, the fibers convert resident moisture into oxidizing agents such as hydrogen peroxide, which have the ability to destroy pathogens. “Since our filter is exceptionally good at absorbing moisture, it can trap droplets that carry viruses and bacteria,” says Forró. “This creates a favorable environment for the oxidation process, which is triggered by light.”
The researchers’ work appears today in Advanced Functional Materials, and includes experiments that demonstrate the membrane’s ability to destroy E. coli, the reference bacterium in biomedical research, and DNA strands in a matter of seconds. Based on these results, the researchers assert – although this remains to be demonstrated experimentally – that the process would be equally successful on a wide range of viruses, including the coronavirus.
Their article also states that manufacturing such membranes would be feasible on a large scale: the laboratory’s equipment alone is capable of producing up to 200 m² of filter paper per week, or enough for up to 80,000 masks per month. Moreover, the masks could be sterilized and reused up a thousand times. This would alleviate shortages and substantially reduce the amount of waste created by disposable surgical masks. Finally, the manufacturing process, which involves calcining the titanite nanowires, makes them stable and prevents the risk of nanoparticles being inhaled by the user.
A start-up named Swoxid is already preparing to move the technology out of the lab. “The membranes could also be used in air treatment applications such as ventilation and air conditioning systems as well as in personal protective equipment,” says Endre Horváth, the article’s lead author and co-founder of Swoxid.

Source: Titanate Nanowire Mask Filter Can Kill Bacteria and Viruses Including SARS-CoV-2/COVID-19

G. Concerns & Unknowns

1. Obesity Raises the Risk of Death From C19 Among Men

The coronavirus has been an unpredictable foe from the start. It triggers silent or barely perceptible infections in some individuals, while in others it sets off a cascade of complications that overwhelm the body and lead to death.
Why some patients sail through the disease and others are felled by it is a question that has bedeviled doctors.
Older age and chronic health conditions like high blood pressure and heart disease are known to increase the risk of severe C19. The Centers for Disease Control and Prevention also lists extreme obesity as a high risk.
But is excess weight in and of itself to blame? Or all of the health problems that accompany obesity, like metabolic disorders and breathing problems?
A new study points to obesity itself as a culprit. An analysis of thousands of patients treated at a Southern California health system identified extreme obesity as an independent risk factor for dying among C19 patients — most strikingly, among younger and middle-aged adults 60 and younger, and particularly among men. [Read the study here]
Among women with the illness, body mass index — a measure of body fat based on height and weight — does not appear to be independently associated with an increased risk of dying at any age, the authors said, possibly because women carry weight differently than do men, who tend to have more visceral and abdominal fat. The study was published in Annals of Internal Medicine on Wednesday.
“Body mass index is a really important, strong independent risk factor for death among those who are diagnosed with C19,” said Sara Tartof, the study’s first author, a research scientist at Kaiser Permanente of Southern California.
But “the impact is not uniform across the population,” she added. “You don’t really see it for the older ages, and we didn’t see it as an important risk for females at any age.”
Obesity and the coronavirus are a dangerous combination for a number of reasons.
Obesity causes restricted breathing, making it more difficult to clear pneumonia and other respiratory infections. Fat is biologically active and a source of pro-inflammatory chemicals, promoting a state of chronic inflammation in the body even before C19 sets in. Obesity causes metabolic changes and abnormalities, even in the absence of diabetes.
The study is not the first to finger obesity as a culprit in C19 deaths in younger people. While early reports from China and Italy did not focus on obesity as an independent risk factor, physicians in other parts of the world, where obesity is more prevalent, were quick to notice that younger individuals who became very ill were often obese.
Only 6% of the Chinese population is obese, compared with 20% of the population in Italy and 24% in Spain. The United States, by contrast, has one of the highest rates of obesity in the world.
Some 42% of American adults have a body mass index of 30 or more, which classifies them as having obesity, and 9% have a B.M.I. of 40 or more. (Someone who is 5’9’’ tall and weighs 270 pounds or more has a BMI of 40, according to federal guidelines.) An individual of that height at 304 pounds has a B.M.I. of 45.
Normal weight ranges from a B.M.I. of 18.5 to 24.9; people with B.M.I.s of 25 to 29.9 are considered overweight.
A report issued by Public Health England concluded that being overweight or obese increased the risk of complications and death from C19. Hundreds of similar articles on the topic have been published.
Among them was a study last month from Columbia University, also published in Annals of Internal Medicine, which found that individuals with C19 who were extremely obese were 60% more likely to require mechanical ventilation or to die from C19. The study noted that this was also the case for people under age 65.
“Is it just that we in the United States have more obese people, so we’re seeing this?” said Dr. David Kass, a professor of medicine at Johns Hopkins University who wrote an editorial accompanying the new study.
“But this is beyond the proportion that would just be in the general population,” he said. “It’s not just that there are a lot of fat people, so we’re seeing a lot of fat people who are very sick.”
Dr. Kass wrote a letter in the Lancet in April noting that many younger C19 patients admitted to American hospitals suffered from obesity, and predicting that as the coronavirus spread through areas where obesity was more prevalent, more younger people would be affected.
The disparate effect on men who are obese is also understandable, he said, because of differences in fat distribution. “If you take a man and woman side by side with the same B.M.I., the male is much more likely to have the background problems that we think are a component for being more at risk,” Dr. Kass said.
To carry out the new study, researchers analyzed the health records of 6,916 members of the Kaiser Permanente Southern California Health System who were treated for C19, both as inpatients and outpatients, from mid-February to May 2.
The median age of the patients was 49 years, and the mean B.M.I. of the patients was 30.6; nearly half were obese.
In general, obesity rates vary by race and ethnicity, according to the CDC. The age-adjusted obesity rate among Blacks is 49.6%, compared with 45% among Hispanics, 42% among whites and 17% among Asian-Americans.
Just over half of the Kaiser Permanente patients were Hispanic, about 1,000 were Asian/Asian-American, and 584 were Black. Many patients had underlying health problems that are linked to poor C19 outcomes. Some 206 — or 3% — of the patients died within 21 days of receiving a C19 diagnosis.
To figure out whether obesity, in and of itself, was associated with a higher death risk, the researchers tried to factor out conditions like high blood pressure and diabetes, which are known to be associated with more severe forms of C19, as well as heart, kidney and chronic lung disease.
The scientists also wanted to know whether demographic factors, like age, sex and race or ethnicity, played a role.
While Black and Latino populations have been disproportionately stricken by the virus, with hospitalizations and deaths at higher rates, the study did not find race or ethnicity to be an independent risk factor.
The researchers did find extreme obesity to be a strong independent risk factor for worse outcomes. “We’re not saying the disparities don’t exist — we’re teasing apart what’s driving the disparities,” Dr. Tartof said.
“We see that racial and ethnic minorities are having more bad outcomes. They are also more likely to be obese, or to have less access to health care, and they’re more likely to have co-morbidities.”
Among C19 patients in the study, those with extreme obesity — defined as a B.M.I. of 40 or more — were at nearly three times greater risk of dying than those of normal weight. Those with a B.M.I. of 45 were more than four times more likely to die than patients of normal weight, with the risk most striking among men and those under 60, Dr. Tartof said.
The study draws attention to the intersection of two major health concerns, Dr. Tartof said, underscoring the need for policies to tackle both.
“There is a lot of work we can do to better combat Covid, and a lot we can do to improve our strategies on obesity as well,” she said. “It is also an epidemic, and something we need to pay attention to.”

Source: https://www.nytimes.com/2020/08/14/health/C19-obesity.html

2. C19 poses a riddle for the immune system

A dysregulated immune response, a cytokine storm and cytokine-release syndrome are some of the terms used to describe the overexuberant defence response that is thought to contribute to disease severity in certain people who become seriously ill with C19. However, a precise definition of this type of immune dysfunction remains elusive. Writing in Nature (here), Lucas et al. fill in some gaps in our knowledge.
A holy grail of C19 research is the ability to assess a person’s immune response, to pinpoint early the individuals who have mild symptoms but who are on track to develop the intense defence response that is associated with severe disease. This is important because there is a broad spectrum of clinical disease in people infected with SARS-CoV-2, the coronavirus that causes C19: some infected individuals can be asymptomatic, whereas others are at risk of dying, and require hospitalization in an intensive-care unit and use of a ventilator machine to breathe. Identifying those whose dysregulated immune-response signature predicts the development of severe disease would enable them to be monitored more intensively to minimize disease progression.
Lucas and colleagues performed extensive analyses of immune responses over time (longitudinal studies) in 113 people hospitalized with C19 who had moderate or severe disease, and assessed a similar number of SARS-CoV-2-free healthy people as controls. The authors analysed molecules in blood plasma (Fig. 1) and monitored peripheral blood mononuclear cells — white blood cells of the immune system such as CD4 T cells, CD8 T cells and B cells. The longitudinal nature of this study enables conclusions to be drawn that wouldn’t be possible from analyzing cross-sectional studies that don’t follow individuals over time.

The authors found that levels of several molecules that promote inflammation — immunomodulatory molecules termed cytokines, including IL-1α, IL-1β, IFN-α, IL-17A and IL-12 p70 — were higher in all of the people who had C19 than in the healthy controls, providing a ‘core’ C19 signature. Other cytokines, such as IFN-λ, thrombopoietin (which is associated with abnormalities in blood clotting), IL-21, IL-23 and IL-33, were upregulated to a greater extent in people with severe C19 than in those with moderate disease. Several of the molecules upregulated in the core C19 signature, as well as those seen in severe disease, have been identified previously as positively correlated with C19 severity.
Severe disease was characterized by prolonged elevation of many of these molecules, whereas the levels of most of them subsided in people with moderate disease. Moreover, individuals with severe disease showed increased levels of cytokines associated with activation of a protein complex called the inflammasome, a component of the immune response that is a driver of inflammation. Also increased were levels of IL-1Ra, a protein that normally inhibits excessive inflammasome function, providing a rare example of an upregulated molecule that dampens the immune response in severe disease.
Levels of molecules associated with a defence response to viral infection — released by a type of activated CD4 T cell called a TH1 cell — were higher in people with severe disease than in those with moderate C19. This occurred even though blood levels of CD4 T cells and CD8 T cells, which are generally linked to expression of these molecules, were similarly decreased (a condition called lymphopenia) in people with moderate or severe disease. More remarkably, cytokines associated with immune responses to fungi (cytokines released by a type of CD4 T cell called a TH17 cell) were elevated and remained so in people with severe disease.
The same was true for cytokines associated with immune responses to parasites, including worms, or with allergic reactions (cytokines such as IL-5, released by a type of CD4 T cell called a TH2 cell). The discovery that parts of the immune system unrelated to viral control would be triggered by a viral infection was unexpected. Less surprising was the finding that levels of inflammatory cytokines in the blood, especially the proteins IFN-α, IFN-γ, TNF-α and TRAIL, correlated with viral RNA levels in the nasal passage, independently of disease severity.
From their analysis of proteins in people’s peripheral blood mononuclear cells, the authors divided individuals into three groups on the basis of their subsequent clinical course and disease severity. In general, at early time points after infection, those who went on to have moderate disease had low levels of inflammatory markers and a rise in the level of proteins associated with tissue repair. By contrast, people who went on to develop severe or very severe disease had increased expression of IFN-α, IL-1Ra and proteins associated with TH1-, TH2- and TH17-cell responses, even at early time points (10–15 days after the onset of symptoms). These results were validated using data for the entire patient population, across all time points, thus demonstrating that these characteristic expression patterns persisted over time in people with each type of disease severity.
What have we learnt from this report, and what still needs to be done? It is clear from this and other studies that the immune response in hospitalized patients with severe C19 is characterized by lymphopenia and the expression of molecules associated with ongoing inflammation, whereas these same molecules are expressed at a lower level in people with mild or moderate disease. Differences in immune responses between the different categories of disease severity are even more evident when people with very mild or subclinical disease are included in the analyses.
A key next step will be to analyse samples from people with extremely early signs of C19, and to compare longitudinal data in those who do and those who don’t require hospitalization. Some people who develop severe disease seem to have a suboptimal immune response initially, which might allow uncontrolled viral replication. Such high replication might, in turn, contribute to severe disease.
Further analyses should identify molecules that are useful for predicting which individuals will later be hospitalized and require intensive care. It will also be crucial to understand how severe disease results in an upregulation of cytokines usually linked to the immune response to parasites and allergic reactions, and whether this apparent dysregulation of the immune response to viral infection is unique to C19. It will also be worth determining whether these changes in the expression of inflammatory molecules in the blood also occur in cells at the site of infection — the airways and lungs. Lucas et al. analysed blood samples because obtaining cells from an infected lung is much more tricky and results in the production of aerosols that might contain the coronavirus.
For results to be clinically useful, it will be necessary to define a limited number of biomarkers that can be both readily measured and used to predict disease outcomes. This could be difficult, because many of the changes in cytokine expression observed in studies such as that of Lucas and colleagues are useful for population-level analyses but less so for predicting outcomes in individual patients. Levels of specific cytokines vary substantially between people, making it hard to benchmark a level of cytokine expression that constitutes a sign of abnormality. Therefore, groups of cytokines, each with different degrees of inter-individual variability, must be measured to identify useful alterations.
The identification of infected people on course to develop severe C19 will be a key step forward in patient care. For example, it would increase the possibility of correctly selecting individuals most in need of targeted early treatment, such as with therapies that directly inhibit viral replication. There has been progress in identifying such treatments, and the continued development of antiviral drugs that have increased efficacy and specificity will be crucial for alleviating the disease and reducing the death rate associated with the C19 pandemic. Ideally, such drugs will be administered orally, and will reduce the need for hospitalization. Continued progress in unravelling the immune response to the coronavirus. infection will help to improve clinical treatments for C19.

Source: https://www.nature.com/articles/d41586-020-02379-1

3. Older Children and the Coronavirus: A New Wrinkle in the Debate

A study by researchers in South Korea last month suggested that children between the ages of 10 and 19 spread the coronavirus more frequently than adults — a widely reported finding that influenced the debate about the risks of reopening schools.
But additional data from the research team now calls that conclusion into question; it’s not clear who was infecting whom. The incident underscores the need to consider the preponderance of evidence, rather than any single study, when making decisions about children’s health or education, scientists said.
Some of the household members who appeared in the initial report to have been infected by older children in fact were exposed to the virus at the same time as the children. All of them may have been infected by contacts they shared.
The disclosure does not negate the overall message of that study, experts said: Children under age 10 do not spread the virus as much as adults do, and the ability to transmit seems to increase with age.
“The most important point of the paper is that it clarifies the care with which we need to interpret individual studies, particularly of transmission of a virus where we know the dynamics are complex,” said Dr. Alasdair Munro, clinical research fellow in pediatric infectious diseases at University Hospital Southampton in Britain.
The earlier study was not intended to demonstrate transmission from children to adults, only to describe contact tracing efforts in South Korea, said Dr. Young June Choe, assistant professor of social and preventive medicine at Hallym University College of Medicine and an author of both studies.
Most studies of children’s transmissibility have been observational and have not directly followed infected children as they spread the virus. The few studies to have done so are not directly comparable — their methods, the policies regarding prevention, and the transmission levels in communities all vary widely.
Many studies have grouped together children of widely varying ages. Yet a 10-year-old is likely to be very different from a 20-year-old in terms of infection risk and transmission, as well as in type and level of social activity, Dr. Munro said.
The first study from South Korea did try to document transmission from children directly, but it grouped them in 10-year ranges. Tracing the contacts of 29 children aged 9 or younger, it found that the children were about half as likely as adults to spread the virus to others, consistent with other research.
But Dr. Choe and his colleagues reported an odd finding in the group of 124 children aged 10 to 19: They appeared significantly more likely than adults to spread the coronavirus. Experts told The Times at the time that the finding was likely to be a fluke.
The group of older children was not the same in both studies, but many appeared in both reports, Dr. Choe said. In the latest study, the researchers found only one undebatable case of transmission among older children, from a 16-year old girl, who had returned from Britain, to her 14-year-old sister.
The remaining 40 infected contacts of the older children could all be explained by a shared exposure.
The children with confirmed infections were isolated in hospitals or community treatment centers, and caregivers who had contact with them were required to wear masks, gloves, a full body suit and goggles. The low rate of transmission from older children observed here may not represent what happens in the real world.
The new report does suggest that older children are at least unlikely to transmit more than adults, said Natalie Dean, a biostatistician at the University of Florida, as had been originally claimed.
“There’s no biological explanation for that,” she said. “It didn’t make any sense to me.” Over all, Dr. Dean added, “We’re not seeing a lot of real transmission from children.”
But that may be because most studies have been too small to adequately distinguish between age groups, and because children have been kept at home, away from potential exposures.
Even if the risk of transmission from children is lower, they usually have contact with a great number of other people — more so than the average adult. When schools reopen, these increased exposures create more opportunities to transmit the virus, which may counterbalance their lower propensity to transmit the virus.
Dr. Dean and other experts cautioned against interpreting the scientific evidence so far as saying that children under age 10 simply cannot spread the coronavirus.
But “it’s not true to say that they do not transmit,” said Bill Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health. “You hear people say this, and it’s wrong.”
All available evidence so far makes it clear that older children, particularly those closest to adulthood, may spread the virus as much as adults, he added.
“It’s indisputable that the highest risk of becoming infected and being detected as being infected is in older age groups,” Dr. Hanage said. “I think you have to be really careful before you decide to open high schools.”
Conversations about reopening schools are complicated because so much depends on the level of community transmission and on socioeconomic factors, he and other experts said.
Schools can fuel the influenza virus’s spread to a disproportionate degree, compared with restaurants, bars or places of worship. Children may drive those outbreaks, so closing schools during flu outbreaks makes sense, Dr. Hanage said.
But with the coronavirus, Dr. Hanage said, “closing schools is not expected to provide more bang for the buck than closing other parts of society.” Instead of reopening bars and restaurants along with schools, he said, schools should be prioritized, while bars and restaurants should be closed in order to reduce community transmission and make school reopenings possible.

Source: https://www.nytimes.com/2020/08/14/health/older-children-and-the-coronavirus-a-new-wrinkle-in-the-debate.html

4. How will C19 affect the coming flu season? Scientists struggle for clues

In March, as the Southern Hemisphere braced for the winter flu season while fighting C19, epidemiologist Cheryl Cohen and colleagues at South Africa’s National Institute for Communicable Diseases (NICD) set up a plan to learn from the double whammy. They hoped to study interactions between seasonal respiratory viruses and SARS-CoV-2, which causes C19. Does infection with one change a person’s risk of catching the other? How do people fare when they have both?
But the flu season—and the answers—never came. NICD’s Centre for Respiratory Disease and Meningitis, which Cohen leads, has logged only a single flu case since the end of March. In previous years, the country’s surveillance platforms have documented, on average, about 700 cases during that period, Cohen says. “We’ve been doing flu surveillance since 1984, and it’s unprecedented.”
Some cases probably got overlooked as clinics temporary closed and people with mild symptoms avoided medical offices and clinics, Cohen says. “But I don’t believe it possible that we’ve entirely missed the flu season with all of our [surveillance] programs.” Apparently, travel restrictions, school closures, social distancing, and mask wearing have all but stopped the flu from spreading in South Africa. Similar stories have emerged from Australia, New Zealand, and parts of South America.
The Northern Hemisphere hopes to be so lucky. Few cases in the south might mean little infection spreading north, says Pasi Penttinen, head of the influenza and respiratory illness program at the European Centre for Disease Prevention and Control (ECDC). But if lockdowns and social distancing measures aren’t in place in October, November, and December, flu will spread much more readily than it has in the south, warns virologist John McCauley, director of the Worldwide Influenza Centre at the Francis Crick Institute.
The prospect of a flu season during the coronavirus pandemic is chilling to health experts. Hospitals and clinics already under strain dread a pileup of new respiratory infections, including influenza and respiratory syncytial virus (RSV), another seasonal pathogen that can cause serious illness in young children and the elderly. In the United States, where some areas already face long waits for C19 test results, the delays could grow as flu symptoms boost demand. “The need to try to rule out SARS-CoV-2 will be intense,” says Marc Lipsitch of the Harvard T.H. Chan School of Public Health.
Because the Southern Hemisphere has largely been spared, researchers have little evidence about how C19 might influence the course of a flu outbreak. One big concern is coinfection—people getting C19 and flu at once, says Ian Barr, deputy director of the World Health Organization Collaborating Centre for Reference and Research on Influenza in Melbourne, Australia. “Two or three viruses infecting you are normally worse than one,” he says.
But the consequences of coinfections with SARS-CoV-2 haven’t been thoroughly studied. In April, a team at Stanford University found that among 116 people in Northern California who tested positive for the coronavirus in March, 24 also tested positive for at least one other respiratory pathogen, most often rhinoviruses and enteroviruses that cause cold symptoms, as well as RSV. Only one of the patients had influenza, although there likely wasn’t much flu circulating so late in the U.S. season, says Stanford pathologist Benjamin Pinsky, a co-author. The study didn’t find a difference in outcomes between C19 patients with and without other infections. But it was too small to draw broad conclusions.

Documented flu cases, April through mid-August

C19 control measures dramatically reduced transmission of flu in many Southern Hemisphere countries this season.

Country	2018	2019	2020
Argentina	1,517	4,623	53
Chile	2,439	5,007	12
Australia	925	9,933	33
South Africa	711	1,094	6

To make things more complicated, having one virus can change a person’s chance of getting infected with another. Epidemiologist Sema Nickbakhsh and her team at the University of Glasgow have found both positive and negative relationships between different pairs of respiratory viruses, even after adjusting for confounding factors that would cause two viruses to show up concurrently or at separate times, such as their tendencies to wax and wane with the seasons.
Coinfections with flu and other respiratory viruses are relatively rare, Nickbakhsh says, and the interactions her group has documented between flu and other viruses have suggested protective effects. For example, being infected with one type of flu virus, influenza A, seemed to reduce the chance of also having a rhinovirus, the researchers reported in 2019. (The mechanism behind this effect isn’t yet clear.)
Nickbakhsh is more concerned about RSV, which her team found to have positive interactions with CoV-OC43, a coronavirus species of the same genus as SARS-CoV-2. It’s possible, she says, that having C19 could increase a person’s susceptibility to RSV, or vice versa. Pinning down possible interactions between C19 and other infections requires a large number of patient samples tested for SARS-CoV-2 and other respiratory viruses. Rapid, dual diagnostic tests will be important for both research and treatment decisions, says Benjamin Singer, a pulmonary and critical care physician at Northwestern University. The FDA has issued emergency use authorizations for flu–C19 combination tests developed by Qiagen, BioFire Diagnostics, and the CDC.
The impending winter in the Northern Hemisphere has also brought new attention to flu vaccines, which may keep hospital admissions down as health systems grapple with the pandemic. Flu vaccine manufacturers including GlaxoSmithKline and AstraZeneca have announced production increases for the 2020–21 season. CDC expects to have a record-setting 194 million to 198 million doses—a 20 million–dose increase from last year. Last month, the United Kingdom’s National Health Service announced it would expand the age groups eligible for a free flu shot among both children and adults.
But what if the flu season is minor? Pouring resources into an immunization campaign necessarily subtracts from C19 responses, says Penttinen, whose team provides guidance to European member states on flu vaccination. Still, rates of vaccination have long been “suboptimal” in Europe, he adds. (Rates among older adults—the target population for the flu vaccine in many countries—range from 2% to 72.8%, depending on the country, according to the most recent ECDC data, released in 2018.) “I think the tendency is to say, ‘We should err on the side of caution—putting efforts into at least maintaining if not increasing the influenza vaccine coverage,’” Penttinen says.
The Southern Hemisphere dodging the flu bullet might create even one more blind spot: Less circulating influenza virus means fewer clues about which genetic variants are most prevalent and likely to contribute to the next flu season. The current record-low season creates a genetic bottleneck, McCauley says, and the flu variants that survive “will be presumably the fittest ones,” he says. It’s not clear what variants will dominate when flu, inevitably, rears its head again.
Barr and McCauley, whose institutions are two of the six that collect and analyze flu samples to decide the composition of the next year’s vaccine, say they’ve received fewer patient samples than in previous years.
Insufficient data could lead to a less effective vaccine for the Southern Hemisphere in 2021. The contents of that cocktail must be decided by the end of September. “It’s a little unsettling,” Barr says, “but we’ll do the best we can with the viruses that we have.”

Source: https://www.sciencemag.org/news/2020/08/how-will-C19-affect-coming-flu-season-scientists-struggle-clues

H. The Road Back?

1. Why Americans Should Adopt The Sweden Model On C19

Figure 1 below illustrates the daily mortality attributed to C19 in Sweden, New York, Illinois, and Texas. The figure plots the daily number of deaths per million population. This figure illustrates the rise and fall of deaths from C19 in four different policy environments. The data were obtained from Worldometer.

Sweden: The Control Group

Sweden (blue dots) has served as a control group to compare policies intended to decrease deaths from C19.
Sweden has been unfairly criticized for its policy despite having an outcome more favorable than places with authoritarian lockdown policies. Sweden did not close its schools. Other than stopping gatherings of more than fifty people, the Swedish government left decisions of closing businesses, using masks, and social distancing to the Swedish people.
The government encouraged the use of masks and social distancing, but there were no requirements and there were no penalties for those who declined to follow the advice.
Mortality attributed to C19 hit a peak value of 11.38 deaths per day per million population on April 8, 2020. This mortality was matched on April 15, and mortality has decreased since then.
Daily mortality has been less than one death per day per million population for the previous eighteen days. Cases are very low.
For all practical purposes, the C19 epidemic is over in Sweden. Almost certainly herd immunity has been achieved in Sweden irrespective of any antibody test results. Testing is usually only for IgG antibody and the herd can become immune via IgA antibody or cellular mechanisms that are not detected by the usual testing. Whether C19 will reappear this next fall or winter remains to be seen.

New York: Locking the Barn Door Shut after the Horse Has Already Left

New York (brown dots) has been a catastrophe.
On March 20, 2020, a full lockdown was implemented. Nonessential businesses were ordered to close. Workers in nonessential businesses were ordered to work only from home. Pharmacies, grocery stores, liquor stores, and wine stores were deemed to be essential and allowed to remain open. Restaurants and bars could only deliver to homes.
In addition to the lockdown, nursing homes were ordered on March 25, 2020, to accept patients positive for the C19 virus in transfer from hospitals. On May 10, this order was changed such that patients had to test negative for the virus before being transferred to nursing homes, but the damage had already been done. By April 7, 2020, within three weeks of the nursing home order, a daily mortality of over fifty deaths per day per million population had been reached. This daily mortality rate was almost five times the peak rate observed in Sweden, where no lockdown was implemented.
The New York policy assumed that all human interactions carry the same risk of death by C19. The New York data clearly shows that interactions among young and healthy people have a much different risk than interactions between the young and elderly and interactions among the elderly.
By facilitating the transmission of the virus from hospitals to nursing homes, the rate of spread within the elderly population was maximized, and any possible benefit from lockdown of the young and healthy population was rendered moot.
The general population was kept locked down after the virus had been broadly disseminated among the elderly population.
The decline of deaths from the peak levels in New York, with its harsh lockdown, has followed roughly the same time course as what has been observed in Sweden without any lockdown.
It is unclear whether the lockdown interfered with herd immunity or not. This will not be known until after the economy and schools are completely reopened for at least a month.

Illinois: A Flattened Curve Led to More Deaths

Illinois (gray dots) has more subtle differences from Sweden than does New York.
Illinois also implemented a harsh lockdown on March 20, 2020. There was no nursing home order as in New York. The daily mortality rate increased more slowly than it did in New York and Sweden, reaching a peak of over fifteen deaths per day per million population on May 17, 2020. The daily mortality has declined more slowly than it did in New York and Sweden, and it remains significantly higher than the rates in those places.
The most likely explanation for the Illinois data is that the lockdown did indeed slow the rate of transmission among the young and healthy but also allowed a longer time for transmission from young people to elderly people.
The lockdown appears to have made more deaths from C19 in Illinois than would have occurred without it. Almost certainly herd immunity has not been achieved and will not be achieved until the schools and economy are reopened.

Texas: The Ox Is Slow, but the Earth Is Patient

Texas (gold dots) had very few deaths following a less harsh lockdown than was implemented in New York and Illinois.
Nonessential businesses were closed on March 31. Outdoor activities were permitted. Social distancing was advised but not required.
Governor Abbott was criticized for not squeezing hard enough, but predictions that Texas health care would be overwhelmed by late April failed to materialize. Texas appeared to be a success story, with a much lower mortality, and the state began a phased reopening of the economy on May 1, 2020.
By late June, however, cases of C19 were increasing and the daily mortality rate was creeping up. The general reopening was paused, and some relaxations of measures were rescinded on June 26, 2020.
The Texas daily mortality rate hit a peak of over ten deaths per day per million population on July 31, 2020. The Texas mortality peak is almost bad as the peak rate seen in Sweden, but Texas still has a largely closed economy.
Texans are debating whether schools should be reopened or not. Sweden does not have to worry about its schools, because it never closed its schools. Texas will eventually have to reopen its schools and economy.
It would appear that C19 deaths were deferred rather than prevented by the lockdown. Although the overall C19 mortality is lower in Texas (293 deaths per million population) than in Sweden (570), the current daily mortality in Texas is much higher than in Sweden, so C19 mortality in Texas may catch up to Sweden over the next 30–60 days.
Furthermore, the situation in Texas will likely get worse when the schools and economy are reopened, as they eventually must be. Like the ox and the Earth, the lockdown slowed the transmission of the virus among the young and healthy, but the virus appears to be very patient and will spread when it is able to.

Conclusions

The data suggest that lockdowns have not prevented any deaths from C19. At best, lockdowns have deferred death for a short time, but they cannot possibly be continued for the long term.
It seems likely that one will not have to even compare economic deprivation with loss of life, as the final death toll following authoritarian lockdowns will most likely exceed the deaths from letting people choose how to manage their own risk.
After taking the unprecedented economic depression into account, history will likely judge these lockdowns to be the greatest policy error of this generation.
C19 is not going to be defeated; we will have to learn how to coexist with it. The only way we can learn how best to cope with C19 is to let individuals manage their own risk, observe the outcomes, and learn from mistakes.
The world owes a great debt to Sweden for setting an example that the rest of us can follow.

Source: https://mises.org/wire/why-americans-should-adopt-sweden-model-covid-19

2. Instead of lockdowns, teach people how to socialize safely

Opinion, by Jason Bae

In response to the rising C19 death toll and case counts in the U.S., calls for a national lockdown have been escalating. In an open letter to America’s decision-makers, more than 150 medical professionals urge them to “shut it down now, and start over.” In the letter, they argue that people should “stay home, going out only to get food and medicine or to exercise and get fresh air.”
I empathize with the urgency in their plea for people to stay home. I felt helpless watching patient after patient die from C19 while working in a New York hospital in April. In the Northern California C19 clinic I work in, I continue to see patients infected with and harmed by the virus. I, too, am desperate for this pandemic to end.
But I believe that telling people to stay home and avoid all nonessential social interactions is the wrong way forward. We should instead focus on educating people and helping them socialize safely. Lessons from sex education indicate that this will be a more effective approach.
A national lockdown is politically impossible today given widespread unemployment and the deepening recession, not to mention the federal government’s failure to coordinate a national response and the extreme politicization of the pandemic.
Telling people to stay home will worsen the mental health epidemic brought on by C19. Michelle Obama recently admitted that “there have been periods throughout this quarantine, where I just have felt too low.” She is not alone. Since the pandemic started, loneliness has increased by 20% to 30%, and emotional distress has more than tripled. This is not surprising: Numerous studies have demonstrated deleterious effects of social isolation on physical and mental health.
Without widespread understanding of how to socialize safely, the cooped-up need for social connection will lead to surges of long-awaited get-togethers and new infections when lockdowns end. We have already seen this phenomenon in Florida and Arizona. It is happening across Europe. In the urgent care clinic where I work, I have seen an increasing number of people who developed C19 symptoms after attending an indoor get-together following months of judicious social distancing.
If telling people to stay home isn’t the answer, then how do we slow this pandemic? By helping them socialize safely.
Several months into the pandemic, we know more about the coronavirus, how it spreads, and how to reduce its transmission from person to person. We know that infection via surfaces is uncommon, and that outdoor transmission is even rarer. We know that face coverings and physical distancing significantly reduce the virus’s spread. At a hair salon in Missouri, for example, two stylists with C19 interacted with more than 100 clients and infected none of them, thanks to the salon’s policy of having stylists and clients wear face coverings.
Instead of insisting that people stay home and indefinitely postpone seeing their loved ones and friends, we should be helping people socialize in ways that minimize the risk of spreading C19.
At an individual level, socializing safely means taking into consideration various factors that determine the risk of coming in contact with the coronavirus: wearing a face covering; frequently washing your hands; being aware of how close you are to others, and for how long; the number of nonhousehold contacts you are with; and ventilation.
Putting that into practice looks like this: Hang out outdoors with a few people instead of indoors with many. Wear a face covering when physical distancing is not possible. Stay home at the smallest hint of fever, fatigue, or cough. Don’t share food or drinks. Limit your social circle and consider creating a “C19 bubble” with one or two close households. These relatively simple steps can help us meaningfully connect with one another without significantly increasing the risk of developing C19.
At a community level, people should be educated about the C19 risks associated with various social activities. Going to the grocery store or playing a noncontact sport like tennis are low-risk activities, while going to a bar or attending a crowded indoor religious service are high-risk activities. Such information, though available, is far from being commonplace knowledge.
It is also essential to enable safe socialization by both making it easy and enforcing it. Closing off streets to cars and painting reminders for physical distancing in public parks and stores are a start, but we can do more. Just as lifeguards at a beach or pool monitor swimmers and discourage them from behaving unsafely, public officials should be deployed in crowded places to remind people to socialize safely and make face coverings freely available to those who need them.
And until the pandemic is under control, the highest-risk activities, such as indoor dining or large concerts, should be discouraged, if not banned.
Some may argue that this “socialize safely” message will backfire and lead to more risky social interactions. There are a few reasons that likely won’t be the case.
One comes from another field of public health: sexual health. Proponents of “abstinence only” education worry that comprehensive sexual education, which covers sexually transmitted diseases, condom use, and safe sexual practices — along with abstinence — leads to increased sexual activity among teens. Yet studies have repeatedly shown that the safe-sex curriculum actually reduces rates of unprotected sex, sexually transmitted diseases, and unwanted pregnancies.
In the context of this pandemic, the “safe socialization” approach has proven successful in other countries. In Japan, people are asked to avoid the 3 C’s — closed spaces, crowded places, and close contact. Instead of self-isolating at home, Canadians are encouraged to exclusively hang out with another household in a “double bubble.”
Telling people to stay home backfired early in the pandemic, resulting in protests, premature reopenings, risky social activities, and the worst C19 pandemic in the world. We can avoid making the same mistake if we choose to accept our social and political realities, heed the latest scientific evidence, and help people socialize safely.

Source: Instead of lockdowns, teach people how to socialize safely – STAT

I. Back to School!?

1. An Update to Colleges’ Reopening Plans

The coronavirus pandemic has left higher-education leaders facing difficult decisions about when to reopen campuses and how to go about it. The Chronicle has teamed up with Davidson College’s College Crisis Initiative (C2i) to present reopening plans for nearly 3,000 institutions. (You can still see The Chronicle‘s tracking data, from before the C2i partnership, though that information is no longer being updated.)
Here’s how the national picture breaks down:

But that doesn’t tell the full story. Two-year colleges, for instance, are much more likely than four-year colleges to be planning an online fall.

Statewide decisions, regional differences, and C19-case counts also appear to play a role:

Explore the data in greater detail at the link below.

Source: https://www.chronicle.com/article/heres-a-list-of-colleges-plans-for-reopening-in-the-fall/

2. Schools Are Reopening, Then Quickly Closing Due to Coronavirus Outbreaks

A growing number of schools nationwide are closing temporarily or longer term just days after reopening as the coronavirus pandemic threatens to upend another school year.
Schools in several states, including Indiana, Louisiana, Oklahoma, Tennessee and Georgia, closed to in-person learning this month after students and staffers tested positive for C19. Several superintendents working to reopen schools also have tested positive, and at least one has died.
The campuses are shutting down to in-person learning indefinitely or for a couple of days for deep cleaning.
“Stay at home if you’re sick,” said Tim Hensley, spokesman at Hamilton County Schools in Chattanooga, Tenn., where four school buildings were temporarily closed after reopening last week. “We found in a couple of our cases, people had actually even gone in to be tested but came to school anyway.”
The Hamilton County district is tracking statistics on employee cases and plans to do the same for students starting this week. As of Aug. 17, the district reported 13 active cases of employees testing positive for C19, 35 having contact with someone with the virus and tests pending for 85 others.
In Jefferson Parish, La., Discovery Schools charter network is closing all four of its campuses to in-person learning until Sept. 11 because of coronavirus cases. The charter system of about 2,400 students will move to only remote learning starting Tuesday. In Indiana, Avon Community School Corporation moved students off campus at Avon High School to remote learning after several C19 cases.
Some districts that planned to reopen for in-person learning are closing schools after returning staffers tested positive for the virus in the days before buildings opened to students.
Darron Arlt, superintendent of Plainview Public Schools in Nebraska, announced at an emergency board meeting Aug. 12 that he had tested positive for C19. School was to start the next day but it has been pushed back to around Aug. 27 because he came in contact with other employees.
“Six teachers and two administrators were deemed to be ‘close contacts’ and therefore required to quarantine for 14 days,” said Dr. Arlt. “We plan to mandate masks for staff and are still considering the same for students.”
Since March, when more than 50 million students were forced into remote learning because of the coronavirus pandemic, the U.S. has largely been torn over when and how to reopen schools. The results of remote learning were generally dismal in the spring, but districts have vowed to make the remote experience better in the new school year.
Many districts are offering families a choice between in-person and remote learning, although some in coronavirus hot spots plan to start the first few weeks online only.
David Freeman, superintendent for about a year in Flour Bluff Independent School District in Texas, died Aug. 5 at age 46 after battling health issues, including C19, said spokeswoman Kim Sneed.
Superintendents throughout the country have braced for sporadic closures as schools reopen, but some have been rocked by the sheer number of positive cases and resulting quarantines.
About 1,921 students and staffers in the Cherokee County School District in suburban Atlanta have been quarantined after coming in contact with dozens of others on campuses who tested positive for the coronavirus since school opened Aug. 3. The district has closed three high schools to in-person learning with reopening possible Aug. 31. Families in the district can choose between in-person and online learning; 77% have chosen to learn in person.
Johnathan Ford Turnbull said his two children are in remote learning because the Cherokee district doesn’t require students to wear masks and his household has high-risk family members.
“It just seems crazy,” Mr. Turnbull said of not mandating masks for students. “We have two kids and both of our mothers live with us. Remote learning was a no-brainer.”
Cherokee school officials asked that students be kept home when sick and get tested before returning to class.
“What happens in our community outside of our schools impacts what happens inside our schools and our ability to keep schools open,” the district said in a statement.
A Wall Street Journal/NBC News poll shows that 49% of parents say they are comfortable with their children going back to in-person school, with an equal share saying they are uncomfortable. The Journal/NBC News poll, conducted Aug. 9-12, has a margin of error of plus or minus 3.27% points for the full sample of 900 registered voters.

Source: Schools Are Reopening, Then Quickly Closing Due to Coronavirus Outbreaks

J. Projections & Our (Possible) Future

1. New model predicts COVID outbreaks in 5 new hotspots

Using smart thermometers that collect data about where people have fevers, it’s possible to estimate how many of those fevers might be due to C19—and predict hotspots before patients go to the doctor for coronavirus tests. A new analysis uses that data to map out where cases may soon spike.
Areas in five states may be particularly at risk in the next two to three weeks: Michigan, Missouri, Illinois, Texas, and Washington. The analysis combines fever data with data about how much people in those areas are moving around, potentially spreading the virus. It also looks at how vulnerable they are because of underlying factors such as lack of access to healthcare, unemployment, and eviction risk.

Urban Footprint, a company that makes urban planning software, partnered with Kinsa, the smart thermostat company, to create what they call the C19 Watch List, building on work that Urban Footprint had already been doing to help decision-makers such as state agencies prioritize where to send resources. “That’s really complex in this context because the situation is constantly changing,” says Urban Footprint CEO Joe DeStefano. “What we’re finding is that everyone is constantly just a little bit underwater. Maybe after five months, people are just starting to tread water. So the idea of being able to look out ahead at where risk is likely to be spiking next, based on early indications from fever data—in this case from the Kansas smart thermometer—data like that is really interesting, and I think really valuable.”
Kinsa used the same type of temperature data in early June to predict spikes in parts of the South and West, predictions that were later borne out in testing data. Combining that with movement data and an understanding of which neighborhoods are least prepared to handle an outbreak can help governments understand where to add new testing facilities and other resources on limited budgets.

“It’s not just looking at places with underlying sociodemographic and economic characteristics, it’s looking at those places that are experiencing ebbs and flows and increasing and decreasing levels of economic stress associated with job claims that are shifting every week, or associated with eviction risk that is incredibly high right now due to the collapse of federal protections or food security,” DiStefano says. “It’s all of these different dynamics coming together into a singular view of priority and risk across the landscape.” They plan to continue to add more data, including about economic activity and school reopenings, to help provide a detailed picture that can be used if cases grow even more in the fall.

The company is working directly with some governments, such as the state of Louisiana, to help them track changing factors, and it’s talking to federal agencies that are deciding where in the country to send resources, and working to understand which areas might be most at risk if an outbreak coincides with a disaster such as a hurricane or a wildfire. Some food relief organizations are also using the information to understand where to send food.

The team plans to build a susceptibility index that anyone working on COVID relief can use to view the maps as they evolve. But because the maps could be a critical tool right away, it also began releasing them now, even before the tool is completely ready. The aim is to give officials a simple way to understand a complex set of factors—such as a rise in evictions and foreclosures—that could also spread the virus as more people are forced to live on the street. “The goal here is really to sort of find that signal through the noise when you have these multivariate challenges that, in and of themselves, are difficult to understand,” he says. “You pull them all together, and if we can just build a map, for example, that a decision-maker can squint at and say, we need to distribute resources here, otherwise the bottom will drop out.”

Source: This new model is predicting COVID outbreaks in 5 new hotspots

K. Practical Tips & Other Useful Information

1. How to Better Cope With the Mental Burden and Loneliness of the C19 Pandemic

The C19 pandemic has reshaped social life in the United States, forcing many to suspend activities that were once considered routine.
As cities move in and out of various stages of reopening and closure, people continue to navigate restrictions on when and where they can see their friends and family. And until there is a coronavirus vaccine, they must also grapple with the probability of recurring outbreaks.
For Prof. Ayelet Fishbach of the University of Chicago Booth School of Business, the pandemic only exacerbates the “modern disease” of loneliness. A leading social psychologist, she says there is a responsibility for policymakers to help guide the public through feelings of uncertainty—a responsibility that too many in the United States have failed to meet.
The following Q&A is edited from a transcript of a March 30 interview with Fishbach, the Jeffrey Breakenridge Keller Professor of Behavioral Science and Marketing.

How badly could the crisis exacerbate the problem of loneliness?

When we think about the effect of social distancing on people’s mental health, we are clearly concerned about those who are lonely. While some of us are at home with other people, others are stuck alone, or are not with the people who matter most to them. Loneliness is a modern disease that has concerned social scientists, governments, and health providers for a long time. We are particularly concerned about older people.
Digital connection is one thing that our modern life offers, which is great. If we’d had to socially distance ourselves prior to the internet, things would have been much harder. But online communication is not like physical connection. In our evolution as humans, we didn’t learn to connect over a single medium such as voice or text. We need to be with each other, touch each other, so that we feel connected.
In my own research, I’ve looked at the effects of having a meal with someone. My co-researchers and I find that people tend to have much better relationships, work better with each other, and feel less lonely if they eat with other people. People now have started to have meals with others over online meetings. It’s clearly better than nothing—not to mention that it’s super creative—but it’s a poor substitute. You can’t share your dish or smell theirs.
When we think about who is going to feel lonelier during these times, this might be older people, and those people who don’t have family with them. Unfortunately, those are also the people who are more at risk to begin with. In general, when we study loneliness, we are concerned about effects on people who live by themselves, on older people, and that’s tough, even if they master technology.

How can policymakers help people cope with uncertainty?

Patience is hard, and being patient when you face a lot of uncertainty is even harder. Reminding people that this is temporary and will not last forever will help them to be patient.
My colleagues and I are running a few experiments to understand what makes people more patient and what makes them feel better about uncertainty, and exploring the way policymakers can communicate social-distancing policies in ways that reduce panic without reducing alertness. I believe this is the part we can play—doing research on how to get people to be more patient, helping people understand some ways by which we can all become more patient. It is the responsibility of policymakers to help people know what to expect, and how long to expect it. This is not something that we should expect medical providers to do. This is not on the professionals who are already in over their heads with trying to save people’s lives.
I would not give U.S. policymakers high grades for how this has been handled so far. We don’t see a clear message. We see a few who are reacting with clear instructions and messages that could make us feel more comfortable, but mostly we see lots of contradictory messages and nothing that addresses the concerns about loneliness, about the long-term economic impact, and so on.
Many people face an unresolved question: How long will I have to wait before I can see my family and my friends? The uncertainty people are experiencing might make them feel that it’s going to take forever. This is a scary thought. Policymakers should explain that there is a solution. They should say: We are working together, we are making progress, and we will resolve it. We are going to get our lives back.
I don’t hear enough of policymakers showing people that this is temporary, that we are fixing things. I also don’t hear enough reminders that we are strong, that we have the resources, and that this country is rich and educated. We can cope with a health crisis. I want to hear that from policymakers.

How soon will life go back to normal after the crisis?

My prediction, reading the research that we have in psychology, is that people are going to get back to hugging each other and spending time together and shopping in supermarkets much faster than they anticipate once the crisis is over. Our human nature is designed to bring us back together; we are just not good at being alone. We like to touch each other. We like to be with each other.
But this is certainly a traumatic event, and there will be negative consequences. We will have to look around us and help the people who are suffering more than us from this. People are going to lose their jobs. Some are going to lose people that are close to them, and obviously that is going to be hard.
On the mental health crisis that is unfolding, clearly some people are struggling with just surviving. There are some people with jobs they need to do now from home while taking care of their children, so they can barely add more stuff to their plate. But we do need to check in with the people around us. We do need to talk to older people, people who are alone.
It’s an interesting question to see what will happen with our consumption habits as a result of this crisis. We basically moved everything online. Are we going to go back to the movies, or is our movie watching just going to be online? Are we going to go to concerts again, or just listen to music on Spotify?
Anything that’s about social interaction—such as going to the movies, the theater, concerts, or the mall on a Saturday—my prediction is that we are going to go back to our old ways as soon as we’re allowed to.

Source: https://scitechdaily.com/how-to-better-cope-with-the-mental-burden-and-loneliness-of-the-covid-19-pandemic/

L. Johns Hopkins COVID-19 Update

August 17, 2020

1. Cases & Trends

The WHO C19 Dashboard reports 21.55 million cases (250,285 new) and 767,158 deaths (5,345 new) as of 10:00am EDT on August 17. The global cumulative mortality surpassed 750,000 deaths on August 15, with the second highest daily death total to date—9,989 new deaths. The WHO also reported the second highest daily incidence on August 15—294,386 new cases. The average global daily incidence has been relatively steady over the past 3 weeks at approximately 1.8 million cases per week (~257,000 cases per day).
Total Daily Incidence of New Cases (change in average incidence; change in rank, if applicable)
- India: 61,798 new cases per day (-217)
- USA: 51,201 (-884)
- Brazil: 43,539 (-1,127)
- Colombia: 11,550 (+680)
- Peru: 8,275 (+763)
- Argentina: 6,756 (-86)
- Mexico: 5,983 (-169)
- Russia: 5,045 (-78)
- Philippines: 4,477 (+468; ↑ 1)
- Spain: 4,064* (+0; new) [Note:*Spain’s average daily incidence is not reported for today; this value corresponds to the previous day’s average. Spain’s average daily incidence has not changed since August 13.]
Per Capita Daily Incidence of New Cases (change in average incidence; change in rank, if applicable)
- Peru: 251 new cases per million population (+23; ↑ 2)
- Panama: 247 (+14)
- Colombia: 227 (+13; ↑ 2)
- Brazil: 205 (-5; ↑ 2)
- Bahrain: 203 (-35; ↓ 4)
- Maldives: 197 (-18; ↓ 2)
- Israel: 160 (-1; ↑ 1)
- USA: 155 (-2; ↑ 1)
- Suriname: 152 (-10; ↓ 2)
- Bahamas: 151 (+32; new)
India reported its highest average daily incidence to date on August 15—62,512 new cases per day—before falling slightly. Spain climbed into the top 10 in terms of total daily incidence, and South Africa fell out of the top 10. In terms of per capita daily incidence, Peru is currently the only country reporting more than 250 new daily cases per million population. The Bahamas climbed into the top 10 in terms of per capita daily incidence, and Argentina fell out of the top 10.
The US CDC reported 5.34 million total cases (54,686 new) and 168,696 deaths (1,150 new). In total, 19 states (increase of 4) are reporting more than 100,000 cases. California is reporting more than 600,000 cases; Florida and Texas more than 500,000 cases; New York more than 400,000; and Georgia and Illinois more than 200,000. Puerto Rico is a US territory, but at 194 new daily cases per million population, it would be #7 globally in terms of per capita daily incidence, falling between the Maldives and Israel. For nearly 3 weeks, the US has averaged more than 1,000 deaths per day.
The Johns Hopkins CSSE dashboard reported 5.41 million US cases and 170,178 deaths as of 1:30pm EDT on August 17.

2. Seasonal Influenza

Public health leaders are looking ahead to the upcoming Northern Hemisphere influenza season and trying to anticipate challenges associated with mounting simultaneous seasonal influenza and pandemic responses. The Northern Hemisphere influenza season typically starts around October and peaks between December and February. In the US, the annual influenza season typically causes 9-45 million cases, including 140-810,000 hospitalizations and 12-61,000 deaths. Last season was relatively mild, but that is not necessarily expected to be the case this year. US CDC Director Dr. Robert Redfield warned Wednesday that the US could face its “worst fall from a public health perspective,” due to seasonal influenza and C19 both straining health systems at once. Dr. Redfield encouraged Americans to wear a mask, avoid crowds, maintain appropriate physical distancing (e.g., 6-foot separation), and practice proper hand hygiene, and notably, he emphasized the importance of getting a seasonal influenza vaccination.
Only about 50% of Americans receive their seasonal influenza vaccination in a typical year, but Dr. Redfield hopes to increase that proportion to 65% this year. The CDC usually purchases 500,000 doses of seasonal influenza vaccine to provide for uninsured individuals, but this year, it is acquiring an additional 10 million doses. Despite this investment, some experts are concerned these efforts will not be sufficient. Seasonal influenza vaccination suffers from a number of challenges, including low efficacy on a yearly basis as well as mis- and disinformation spread by anti-vaccine advocates. In order to improve vaccination coverage, health officials have allocated considerable effort and resources to expanding access to the vaccine, including at convenient locations such as schools and workplaces; however, many of these locations may be closed due to social distancing restrictions, which could subsequently limit access for some communities.
The ongoing Southern Hemisphere influenza season has been very mild compared to past years, which some have attributed to social distancing measures implemented for C19. If social distancing can limit seasonal influenza transmission, the Northern Hemisphere could potentially experience a mild influenza season as well, but that would depend heavily on the degree to which communities adhere to social distancing policies.

3. Saliva-Based Diagnostic Test

The US FDA issued an Emergency Use Authorization for a saliva-based diagnostic test developed by researchers at the Yale School of Public Health.
When compared with other FDA-authorized diagnostic tests, the SalivaDirect protocol demonstrated an 83%-100% agreement.
A saliva-based test offers a number of potential benefits over existing diagnostic tests. Collecting a saliva sample is more comfortable than nasopharyngeal swabs, and the SalivaDirect tests can use any sterile container, as opposed to requiring expensive tubes as is the case for some other saliva-based tests. Additionally, the testing protocol is reportedly more streamlined than other diagnostic tests, which eliminates the need for certain reagents and decreases testing time, and the tests require no proprietary supplies to process. Yale researchers are also making the protocol “open source,” so any laboratory can order supplies and follow the instructions rather than purchase tests from a single manufacturer. Test materials are also relatively inexpensive, less than US$5 per test.
Researchers are currently working with the National Basketball Association on the Surveillance with Improved Screening and Health (SWISH) study to determine the test’s ability to detect asymptomatic infections, but the ultimate goal is to expand availability more broadly to supplement existing testing capacity. Additional studies to modify the original protocol to increase testing capacity via automation, pooled testing, and rapid detection are also underway. Additional information about the test, including instructions for use and obtaining authorization to use the protocol, can be found here.

4. US Personnel & PPE Shortages

On Friday, the US FDA published a list of medical device and equipment shortages for the first time during C19 pandemic. The list includes a wide variety of items, including personal protective equipment (PPE), such as examination gloves, surgical gowns, and respirators; swabs and viral culture medium used for testing; and mechanical ventilators. Reporting this information is required under the CARES Act.
A report published by Politico describes findings, based on survey and interview responses from frontline healthcare workers and hospital administrators, regarding the challenges that healthcare facilities are facing in terms of securing necessary supplies and personnel. As we have reported previously, without centralized coordination at the national level to distribute limited resources, hospitals and health systems have been forced to compete against each other. Notably, some smaller hospitals do not have the resources to compete with larger and better-funded facilities, both for supplies and personnel, resulting in shortages of both.

5. Lebanon

Lebanon’s Minister of Public Health announced that the country will require a 2-week “lockdown” to curtail a recent rise in C19 incidence. The recent surge of transmission in Beirut has also complicated response efforts following a major explosion at the city’s port last week that resulted in at least 178 deaths and more than 6,000 wounded and left approximately 250,000 individuals homeless. The government has not yet published details regarding how the lockdown measures will be implemented. To date, Lebanon has reported 9,337 total cases, including 105 deaths, and the daily incidence has nearly ten-fold since early July.

6. Racial & Ethnic Disparities

A study, published in the US CDC’s Morbidity and Mortality Weekly Report, evaluated county-level data for areas identified as C19 hotspots between June 5 and June 18, and the findings provide further evidence of racial and ethnic disparities in C19 incidence. In total, 205 counties across 33 states were identified as hotspots during the study period, of which 79 counties (22 states) reported race/ethnicity data for at least 50% of the reported cases. The researchers defined disparity as either a 5% or greater absolute difference between the proportion of C19 cases among a specific race/ethnic group and the proportion of that group among the general population (e.g., a race/ethnic group represents 15% of C19 cases but only 10% of the population) or a ratio of 1.5 or greater between the proportions (e.g., a race/ethnic group represents 4.5% of cases but only 3% of the population).
Of the 79 included counties, 76 (96.2%) exhibited racial or ethnic disparities for at least one racial or ethnic minority group. These disparities affected minority populations totaling approximately 5.6 million people across the included counties, representing more than 20% of the 27.5 million total population. The most severely affected racial/ethnic groups were Hispanic/Latino and Black/African American populations, totaling 3.5 million and 2 million people, respectively.

7. Lasting Immunity

The US CDC published clarifications on some recent guidance regarding quarantine, isolation, and the possibility of SARS-CoV-2 reinfection. On August 3, the CDC updated its isolation guidance to include new information which indicates that individuals infected with SARS-CoV-2 can “continue to test positive for up to 3 months after diagnosis and not be infectious.” On Friday, the CDC clarified that this does not mean that individuals are immune to reinfection for 3 months. Investigation into lasting immunity and risk of reinfection are ongoing, and while there has not been documented evidence of reinfection within 3 months, the possibility or reinfection during this period has not yet been ruled out.
The previous guidance stated that “People who have tested positive for C19 do not need to quarantine or get tested again for up to 3 months as long as they do not develop symptoms again.” Some interpreted this statement as implying a 3-month period of immunity, so the CDC clarified that its intent was to state “that retesting someone in the 3 months following initial infection is not necessary” due to the possibility of continued positive tests, even after an individual has recovered and is no longer infectious.
The CDC has included updated language about reinfection for multiple guidance pages, including for quarantine and self-isolation.

8. New Zealand Delays Election

New Zealand Prime Minister Jacinda Ardern announced that the country’s general election will be postponed from September 19 to October 17 due to C19, including an ongoing outbreak in the capital city of Auckland. The delay is intended to aid political parties’ ability to plan for campaigning under C19 restrictions. Reportedly, Prime Minister Ardern collaborated with leadership from all major political parties in making the decision, and the decision appears to have broad support among the general public. She indicated that the election date will not be delayed any further due to C19, even if the situation worsens. The outbreak in Auckland is up to 58 total cases, including 9 identified in the past 24 hours.

9. South Korea

After bringing its “first wave” of C19 under control, South Korea is battling another outbreak, this time in Seoul. Early in its epidemic, SARS-CoV-2 transmission largely centered around a religious group in Daegu, and the current surge has been linked to a different religious group in the country’s capital. Over the past 3 days, South Korea has reported 642 total cases reported nationwide, and 553 of these are domestically acquired cases in Seoul and the Gyeonggi and Incheon provinces, which surround Seoul. In total, nearly 450 cases in Seoul, Incheon, and Gyeonggi have been linked to clusters at 2 churches in the Seoul metropolitan area, as well as more than a dozen cases in other parts of the country.

As of August 15, all members of the Woori Jaeil Church in Gyeonggi province (approximately 900 individuals) were in quarantine, and all members of the Sarang Jaeil Church in Seoul who were present August 7-13 were directed to quarantine on August 16. The pastor at the Sarang Jaeil Church has reportedly hindered the public health response, including holding a large protest against South Korean President Moon Jae-in that drew a crowd of 10,000 people. In response to the recent increased incidence, South Korea increased the C19 alert level in Seoul to Level 2 (out of 3), which restricts indoor gatherings to no more than 50 people and outdoor gatherings to 100 or fewer and prohibits fans from sporting events, along with other social distancing measures.

Index

A. The Pandemic as Seen Through Headlines

B. Numbers & Trends

C. Updates

D. New Scientific Findings & Research

E. Improved & Potential Treatments

F. Testing & Masks

G. Concerns & Unknowns

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 (8/17)

M. Links to Other Stories

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 (8/17)

C. Updates

1. 7 months later, what we know about C19 — and pressing questions that remain

What We Know

Covid and kids: It’s complicated

There are safer settings, and more dangerous settings

People can test positive for a long time after they recover. It doesn’t matter

After the storm, there are often lingering effects

‘Long-haulers’ don’t feel like they’ve recovered

Vaccine development can be accelerated. A lot

People without symptoms can spread the virus

Mutations to the virus haven’t been consequential

Viruses on surfaces probably aren’t the major transmission route

What We Don’t Know

People seem to be protected from reinfection, but for how long?

What happens if or when people start having subsequent infections?

How much virus does it take to get infected?

How many people have been infected?

It’s not clear why some people get really sick, and some don’t

2. What if ‘Herd Immunity’ Is Closer Than Scientists Thought?

Virus-Resistant Communities?

Imperfect Immunity

D. New Scientific Findings & Research

1. Mild C19 cases can produce strong T cell response

2. Acupuncture could help coronavirus patients

E. Improved & Potential Treatments

1. NIH Launches ACTIV-3 Clinical Trial to Test Antibody Treatments in Hospitalized C19 Patients

2. C19 Treatment Possible As Preexisting Drug Shows Promise in Fight Against the Coronavirus

How It Works

Drug Development Potential

F. Testing & Masks

1. FDA clears saliva test for C19, opening door to wider testing

2. New C19 Virus-Filtering Mask Material Being Fast-Tracked to Market

3. Titanate Nanowire Mask Filter Can Kill Coronavirus

G. Concerns & Unknowns

1. Obesity Raises the Risk of Death From C19 Among Men

2. C19 poses a riddle for the immune system

3. Older Children and the Coronavirus: A New Wrinkle in the Debate

4. How will C19 affect the coming flu season? Scientists struggle for clues

Documented flu cases, April through mid-August

H. The Road Back?

1. Why Americans Should Adopt The Sweden Model On C19

Sweden: The Control Group

New York: Locking the Barn Door Shut after the Horse Has Already Left

Illinois: A Flattened Curve Led to More Deaths

Texas: The Ox Is Slow, but the Earth Is Patient

Conclusions

2. Instead of lockdowns, teach people how to socialize safely

I. Back to School!?

1. An Update to Colleges’ Reopening Plans

2. Schools Are Reopening, Then Quickly Closing Due to Coronavirus Outbreaks

J. Projections & Our (Possible) Future

1. New model predicts COVID outbreaks in 5 new hotspots

K. Practical Tips & Other Useful Information

1. How to Better Cope With the Mental Burden and Loneliness of the C19 Pandemic