Coronavirus Update 1-20

Recent Developments

January 20, 2021

More severe and more deadly variant of coronavirus may be emerging in Brazil
(see 5^th story under New Variants (Mutations) of Coronavirus)

“Something very different is happening in Manaus. I don’t know if it is a new strain or if it is something different. But those on the front line are seeing an increase in the severity of the cases. And it is not just killing those in a risk group: this is in all age groups, affecting babies, children, teenagers even without comorbidity.”
Silvia Leopoldina, infectologist who also works in the state public networks and municipal of Manaus, Brazil. The doctor says there were changes in the behavior of the disease in the state.

Index

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

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

A. Pandemic Headlines

B. Numbers & Trends

Cases & Tests
Deaths
Top 5 States in Cases, Deaths, Hospitalizations & Positivity

C. New Variants (Mutations) of Coronavirus

D. New Scientific Findings & Research

E. Vaccines & Testing

US Vaccine Distribution
New C19 Vaccine: Nanoparticle Immunization Technology Could Protect Against Many Strains of Coronaviruses

F. Improved & Potential Treatments

G. Concerns & Unknowns

H. The Road Back?

Population density and transmissibility of virus strains will affect how regions can resume normal life

I. Back to School!?

J. Innovation & Technology

N. Johns Hopkins COVID-19 Update

O. Linked Stories

Notes:

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A. Pandemic Headlines

(In no particular order)

Fauci: New COVID-19 vaccines could be ‘weeks away’ from possible approval
Biden’s CDC pick projects grim COVID death toll by mid-February
Israel’s Fauci says Pfizer vaccine’s first dose less effective than indicated
Immune system ‘remembers’ to fight off coronavirus for at least 6 months: study
West Virginia leads nation in vaccine distribution
Alabama’s COVID-19 vaccination efforts ranked last in US
NYC will run out of its current vaccine supply on Thursday, the mayor says. It’s not scheduled to get more until next week
13,000 NY Nursing Home Residents And Nearly Half Of Staff Decline COVID-19 Vaccine
27 percent of New Yorkers say they won’t get COVID vaccine: poll
California’s nightmare surge may be receding, but a new variant and a jumbled vaccine rollout could threaten progress
A new California variant may be driving the virus surge in the state, a study suggests
18 family members get COVID-19 after holiday gathering
Los Angeles County hits 1M COVID cases despite strict lockdowns
UK considering “all possible measures” as deaths spike
Germany tightens lockdown ‘to prevent the danger that lies in this mutated virus
Germany extends lockdown to Feb. 14
UK Authorities Could Force People To Take Selfie Every Day To “Prove” They’re Self-Isolating
The COVID-19 Pandemic Has Overwhelmed the Health Systems in Brazil
Japan’s southernmost prefecture, Okinawa, declared a state of emergency after a spike in cases
Scotland’s lockdown will be extended to mid-February and its schools and kindergartens will remain closed until then
China Reports 100+ New Cases For Sixth Day As Lockdowns Expanded To 29 Million
Germany to hold COVID quarantine violators in detention centers
Brazil approves US, Chinese vaccines
Japan’s suicides jump 16 percent in COVID-19 second wave
Health care workers admitted China lied about COVID-19, documentary claims
Independent Panel Hired by WHO: China, WHO should have acted quicker to stop pandemic
‘Catastrophic moral failure’: WHO slams COVID vaccine distribution
The E.U.’s executive arm sets its goal: 80% of people over 80 and 80% of health care workers to be vaccinated by March
Russia mulls ‘Covid passports’ to let people with some immunity travel more easily
EU Kicks off Debate on Vaccine Travel Certificates
Research: 890,000 Americans may die due to COIVD lockdowns
COVID-19 surge increases strain on funeral homes
LA suspends air-quality limits on crematoriums to cope with COVID-19 bodies
10,000 Protesters In Vienna March Against Coronavirus Restrictions
French Workers Angrily Reject Social Distancing “Dog Collars”
Over 50,000 Restaurants In Italy Declare “I Am Open” Defying Lockdown Measures
1000s Denounce COVID Lockdown In Amsterdam As Chaos Unfolds At “Unauthorized” Gathering
Ice Cream From China Contaminated With COVID: Officials
NY still not allowing immunocompromised to receive COVID-19 vaccine
Australian Open’s COVID-19 outbreak is getting worse
VIPs flock to maskless, 150-guest private concert in Miami
Airbnb CEO Warns Travel ‘Will Never Go Back To Normal’
Gov. Noem’s No-Lockdown Win: People Moving To South Dakota in Droves
“People Are Nearing Rock Bottom”: Fed’s COVID Response Rewards Wealthy While Brutalizing Nation’s Poorest
Some prisons are offering skeptical inmates incentives to consent to vaccination
The SAT is dropping its essay section and subject matter tests to streamline during the pandemic

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 = 96,602,564
New Cases (7 day average) = 656,572

Observations:

7 day average has been declining at a rapid rate since 1/11
Since 1/11, the 7 day average has decreased from 738,738 to 656,572, a decline of 11.1%

US Cases

Total Cases = 24,809,841
New Cases (7 day average) = 204,228
Percentage of New Global New Cases = 31.1% (US = 4% of world population)

Observations:

7 day average has been falling at a rapid rate since 1/11
Since 1/11, the 7 day average has decreased from 254,858 to 204,228, a decline of 19.9%

2. Deaths

Worldwide Deaths:

Total Deaths = 2,064,015
New Deaths (7 day average) = 13,444

Observations:

7 day average has declined slightly from its record high of 13,659 on 1/17

US Deaths:

Total Deaths = 411,520
New Deaths (7 day average) = 3,098
Percentage of Global New Deaths = 29.6% (US = 4% of world population)

Observations:

7 day average has dropped sharply since its record high on 1/16
Since 1/16, the 7 day average has decreased from 3,420 to 3,098, a decline of 9.4%

3. Top 5 States in Cases, Deaths, Hospitalizations, ICU Patients & Positivity (1/19)

https://lh5.googleusercontent.com/2lC7ui60ZDDkjjJt7t7S2_rGh3GuVnDfnsSe9m0reN-i7KClXQNVcGkXaiDXRpBUHOfDapP_ZO-WYI6kRb_tmco0tTBgSqwwhR5w2GMlUkBa7fUwVPW68qfhUTh68mwd0fu-G61B

https://lh6.googleusercontent.com/vxIgc-V7JGAlpyFr-k2yelIPeWc0C7bB0mQCjVy4rsQLm_qxqUTRMlLGFi-WN3JnPtgNdT2-U7k_nNbLM2QJCDfmAFlKQm5XZDwe6oqJjzmxWbCZBjl2yptteHBZoSwXINEg4rjo

Observations

It would appear that the US has crossed over the holiday peak:
- Positivity rates continue to decline across the US.
- Hospitalizations and Patients in ICU both reached the lowest levels since the start of 2021.

Positivity Trends

The US Positivity Rate fell to 12.8%, it’s lowest level since 12/28. It marks its 11th straight decline since peaking at 17.2% on 1/8 .
- Only 4 states (MS, OR, VA, NE) reported higher positivity rates over the last week (-10 states since 1/12).
- WY leads the US with an average of 49.8% of all tests resulting positive
- Three states: 7-day positivity rates greater than 40% (-5 since 1/12)
- Eight states: 7-day positivity rates greater than 30% (+2 since 1/12)
- Eleven states: 7-day positivity rates greater than 20% (unch since 1/12)
- Three states (AK, MS, CT): 7-day positivity rates less than 5%. (unch since 1/12)
- In total, 47 states have 7-day positivity rates greater than 5% (unch since 1/12)

Hospitalization Trends

Hospitalizations fell during the last week 5.7% to 123,820 patients. This represents the lowest level since 1/3.
- Two states have had increases of hospitalized patients of more than 10% in the past week. (-2 since 1/12)
- 28 states have more than 1,000 hospitalized patients (-1 since 1/12).
- 45 states saw decreases in the number of hospitalized patients over the past week. (+15 since 1/12).

Patients in ICU Trends

The number of patients in the ICU fell during the last week 3.6% to 23,029 patients. This represents the lowest level since 12/30.
- Four states have seen the number of ICU patients increase by more than 10% since a week ago (-1 since 1/12).
- 29 states have more than 100 patients in ICU, (+1 since 1/12).
- 29 states saw decreases in the number of ICU patients over the past week (-7 since 1/12).

C. New Variants (Mutations) of Coronavirus

1. What we now know—and don’t know—about the C19 variants

Below, STAT explains what’s known about the variants, why they’re getting so much attention, and what they mean for the trajectory of the pandemic.

Why are variants popping up now?

The coronavirus (SARS-CoV-2) has been mutating all along; that’s just what viruses do. Many of those mutations don’t change the virus substantively, and some might actually be detrimental to the virus, making that variant likely to die out.
But every so often, a mutation or combination of mutations will give rise to a new form of the virus with an evolutionary edge, like being able to infect cells better or spread faster. This new variant can outpace earlier iterations of the virus and become dominant.
Early on in the pandemic, a mutation known as D614G seems to have given the virus a boost in its infectiousness, and variants with the mutation became the most prevalent around the world.
Beyond the fact that the virus is constantly changing, there are other reasons why these “fitter” variants have started to emerge. In the early days of the pandemic, when just about all of us were vulnerable to C19, any infectious variant had a pretty easy time circulating. But as more people in certain areas have become protected — either after an initial infection or vaccination — pressure on the virus has increased. A so-so spreader might no longer be able to find new hosts (that’s us) to infect, but variants with mutations that help them spread can still transmit, and can take off from there.
“We’ve reached a point one year on and in certain parts of the world where the density of natural immunity is sufficient so that the variants that have got a fitness advantage … are more likely to emerge and spread,” said Wendy Barclay, the head of infectious diseases at Imperial College London.
The variant that first appeared in the U.K. — and perhaps others as well — is a bit of a special situation. Most people who have an acute case of C19 will vanquish the virus after a relatively short period of time. But it’s thought that this variant, dubbed B.1.1.7, came from a person who was immunocompromised and had a rare chronic case, essentially providing an incubator for the virus to accrue mutations as it replicated for weeks or months in that person’s body. The virus, the hypothesis goes, then spread from that person to others.

If the virus is changing all the time, why are these variants setting off alarms?

For now, let’s focus on the variants that emerged first in the U.K., South Africa, and Brazil. (There are at least two variants in Brazil scientists are keeping an eye on). These have the most evidence of greater transmissibility or some other characteristic that might be cause for concern. And, what’s more, they share some of the same mutations despite arising independently. To scientists, that’s a clue that the mutations might confer some evolutionary advantage.
When scientists assess the impact of a new viral variant, they consider at least three factors: disease severity, protection, and transmissibility.
For now, none of the variants seems to change how sick people get with C19.
Answering the question of whether people with existing immunity to SARS-2 are still protected — and whether the vaccines still work — is a bit more complicated. Scientists are testing vaccines against the mutations and variants, and results should be available in the coming weeks. But many experts have a fairly optimistic outlook on the vaccine question. The vaccines generate a multipronged immune response that recognizes and targets different parts of the virus; changes caused by one mutation likely won’t make the virus invisible to protective antibodies generated by immunizations. And even if a mutation reduces the vaccines’ effectiveness a bit, the shots have been shown to be so powerful that they should work just fine even if their potency is taken down a notch.
Eventually, scientists think, the virus will accumulate the right combination of mutations to warrant updating the vaccines, a not-that-difficult process for vaccine makers. But it doesn’t appear we’re at that point now (though plenty of studies are ongoing, and some are more anxious than others).
There are some concerns about people becoming more vulnerable to reinfection with the new variants. In lab experiments, one of the mutations present in the variants identified in South Africa and Brazil, called E484K, has helped the virus evade the antibodies generated after an initial infection in some people.
On Monday, scientists in South Africa reported that antibodies from some people infected during the country’s first wave failed to recognize the newer variant spreading there now; they didn’t have results yet about its impact on vaccine-elicited antibodies. Separately, in Brazil, surging cases in a region that had already been hit hard by the virus raised worries that a different variant, called P.1, is able to sneak past existing protection and infect people again.
When it comes to transmissibility, it seems that these variants do spread more easily — though there are wide-ranging estimates for just how much more infectious they are.

What does a more transmissible virus mean?

Because a more transmissible variant can infect more people more quickly, it leads to more cases overall without mitigation efforts. Even if people individually aren’t likely to get sicker, the result is that there will be more hospitalizations and deaths. (One caveat: Widespread vaccinations could prevent some of those.)
Faster-spreading viruses also require a greater proportion of a population to be protected for herd immunity to be achieved. Vaccine campaigns will have to reach even more people.
That also means that more contagious variants can spread in communities that, even if they hadn’t hit herd immunity, had enough immune people to blunt the circulation of SARS-2.
The arrival of more transmissible variants is “bad news, because that means some places that had already started to see protective effects become vulnerable again,” said Caitlin Rivers, an infectious diseases epidemiologist at the Johns Hopkins Center for Health Security.

What’s happening in Brazil?

A recent study estimated that 75% of residents of the city of Manaus, Brazil had been infected by SARS-2 by October. The hope was that this level of protection might act as a buffer against more transmission. But last month, cases started rising in the city and its state of Amazonas, straining local health systems once again.
When researchers dug into the viral sequences, they found many cases involved a new variant, called P.1, as reported last week. (P.1. has also been identified in people who traveled from Brazil to Japan.) They warned the mutations it contained (including E484K) are “potentially associated with an increase in transmissibility or propensity for re-infection of individuals.”
Maybe P.1 is indeed able to evade some existing immune protection, leaving people more susceptible to reinfection. Scientists on Sunday confirmed a case of reinfection caused by P.1 in Amazonas.
Or perhaps P.1 is so transmissible that it can spread just fine even in communities with 75% protection.
Or what if some people in Amazonas who were infected months ago are just generally becoming susceptible again to any form of reinfection, regardless of variants?

What are scientists doing about all this?

Studying it from all angles. One line of inquiry is examining the effects of mutations in isolation and in concert with the other changes dotting the virus’ RNA genome. Essentially, a mutation on its own may not have much of an impact, but it can help a virus spread better or replicate faster if it’s paired with certain other mutations.
Scientists are also on the lookout for other potential variants of concern as they comb through sequencing data. But there’s a sense among some experts that new variants are being announced without much helpful information. Lots of mutations will be discovered; it can take some time to figure out what, if anything, each one means.

And what can I do about it?

Commit to the same precautions that have been recommended for months, experts say. Perhaps invest in a better mask than a fabric face covering. Get vaccinated when you can.

Source: https://www.statnews.com/2021/01/19/coronavirus-variants-transmissibility-disease-reinfection/

2. Fauci warns of ‘more ominous’ strains of C19 from Brazil, South Africa

Dr. Anthony Fauci warned that “more ominous” strains of C19 have emerged out of South Africa and Brazil.
The Director of the National Institute of Allergy and Infectious Diseases said they’re looking “very carefully” at the two new mutant variants in addition to another highly-contagious one that was first detected in the United Kingdom.
“People need to realize there’s more than one mutant strain,” Fauci told NBC anchor Chuck Todd on “Meet the Press.”
“There’s one from the UK that’s essentially dominated… There’s another more ominous one that’s in South Africa and Brazil.”
Fauci said he doesn’t want “people to panic,” but they’re taking the new strains “very seriously” and studying them to fully understand the threat that they pose.
“The Brits have made it very clear that [the strain detected there is] more contagious,” Fauci said.
“They say that it isn’t more virulent. But, you know, we’ve got to be careful because the more cases you get, even though on a one-to-one basis it’s not more virulent, meaning it doesn’t make you more sick or more likely to die, just by numbers alone the more cases you have, the more hospitalizations you’re going to have.”
He said they’re still determining whether these mutations will be resistant to the vaccines on the market.
“The thing we really want to look at carefully is that does that mutation lessen the impact of the vaccine?” he said. “And if it does, then we’re going to have to make some modifications… We’re looking at that really very carefully.”

Source: https://nypost.com/2021/01/17/fauci-warns-more-ominous-strains-of-covid-19-have-emerged/

3. Another coronavirus variant linked to growing share of cases, several large outbreaks, in California

A coronavirus variant first identified in Denmark has ripped through Northern California — including outbreaks at nursing homes, jails and a hospital in the San Jose area — prompting state and local officials to investigate whether it may be more transmissible.
California officials disclosed the rise of the variant Sunday night after genetic monitoring linked it to a fast-growing share of new cases, as well as to the outbreaks in Santa Clara county, which includes San Jose.
This rising variant is distinct from the highly contagious mutation discovered by Britain, which has also been found in California, and which federal health officials project could become the dominant strain in the United States by March based on its proven higher transmissibility.
Experts stress that they need to look more closely at the circumstances of the Northern California outbreaks, as well as at the latest variant — this one, known as L452R — before declaring it more contagious or more dangerous than the virus already broadly circulating.
The L452R variant was first detected in northern Europe in March and has since been confirmed in more than a dozen states, including California in May. The discovery did not garner much attention at the time because all viruses change constantly as they replicate. But public health authorities deem some variants to be “of concern” if evidence suggests they might be more contagious, potentially deadlier or resistant to vaccines.
California publicized the latest variant at a late Sunday news conference after researchers identified it in about 25% of samples collected between Dec. 14 and Jan. 3, a surge from 3.8% of samples collected in the preceding three-week period.
“That is suggestive, and it’s a little worrisome,” Charles Chiu, a virologist at the University of California at San Francisco said at the briefing. But Chiu stressed it was too early to conclude the variant is more infectious because scientists do not know whether their sampling was representative or whether the variant’s increase might be due to random chance, or even a series of superspreader events.
Officials urged people to follow public health guidelines to minimize the risk of contracting the variant as new daily cases in the hard-hit state plateau at more than 38,000, while deaths average more than 515 daily.
“It’s too soon to know if this variant will spread more rapidly than others,” said Erica Pan, California’s state epidemiologist, “but it certainly reinforces the need for all Californians to wear masks and reduce mixing with people outside their immediate households to help slow the spread of the virus.”
Genetic sequencing of viruses is still limited in the United States, preventing health officials from having a real-time picture of all the strains of coronavirus spreading across the country and their prevalence.
California’s preliminary data is based on fewer than 400 samples that overwhelmingly came from the state’s north. Southern California is the heaviest hit part of the state, with deaths in Los Angeles County reaching one every seven minutes and ICU beds and oxygen running out, although hospitalizations have begun to plateau. Environmental regulators on Sunday temporarily lifted limits on cremations because of a backlog in Los Angeles County.
The L452R strain in California raised alarms because it is associated with several large outbreaks in Santa Clara County, including one at a hospital that infected at least 90 people and killed one staff member. Officials at Kaiser Permanente San Jose Medical Center said a staff member wearing an inflatable Christmas tree costume to spread holiday cheer likely spread coronavirus-laden droplets instead.
Sara Cody, Santa Clara’s top public health official, described that episode as a “very unusual outbreak with a lot of illnesses, and it seemed to spread quite fast.” The county is working with state health officials and the CDC to investigate what happened, she said.
Cody cautioned that the outbreak could have been driven by factors unrelated to the variant, such as changes in ventilation or personal protective equipment practices at the hospital.
“The takeaway is not that we need to start worrying about this,” Cody said Sunday. “The takeaway is, this is a variant that’s becoming more prevalent, and we need to lean in and understand more about it.”
County officials on Monday disclosed other places where the variant had been found as a result of aggressive genetic sequencing, “including cases associated with the Kaiser outbreak, skilled nursing facility outbreaks, cases in jails and shelters, and specimens from testing sites in the community,” according to a statement. “This suggests that the variant is now relatively common in our community.”
Chiu, the virologist who conducted the genetic sequencing, said a deeper investigation must be done to determine if the strain is more transmissible like the one found in the United Kingdom.
He also raised concerns that a mutation associated with the variant might make it more resistant to vaccines because it occurs in a critical part of the spike protein that is targeted by the vaccines, but he added that the virus must be grown in a lab and tested more fully before any conclusions can be drawn.
“Mutations happen all the time,” said William Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health. “Some of them take off and the great majority of them don’t. The main reason why we are paying attention to this is because this mutation has previously been noted as being of particular concern in terms of diminishing the efficacy of the immune response.”
Carlos del Rio, a professor of medicine and global health at Emory University, said the rising prevalence of the variant shows the urgent need for more genetic sequencing in the United States and for greater compliance with public health measures such as wearing masks and avoiding crowds.
“We really need to hunker down because if you are really concerned about mutations, stop transmission,” del Rio said. “The more mutations you see, the more uncontrolled transmission you will see.”
After starting the new year with record-high cases, deaths and hospitalizations, the United States is starting to see signs of slowing spread despite fears of a post-holiday surge that would continue through January. The seven-day average of new infections has slowed since last Tuesday, and hospitalizations have started to plateau, according to Washington Post tracking.
Still, Scott Gottlieb, a former Food and Drug Administration commissioner, warned that the advent of more transmissible variants could reverse that progress.
“As current epidemic surge peaks, we may see 3-4 weeks of declines in new cases but then new variant will take over,” Gottlieb tweeted Sunday, referring to the British variant. “It’ll double in prevalence about every week. It’ll change the game and could mean we have persistent high infection through spring until we vaccinate enough people.”

Source: https://www.washingtonpost.com/health/2021/01/18/california-coronavirus-variant/

4. A Troubling New Pattern Among the Coronavirus Variants

For most of 2020, the coronavirus jumped from human to human, accumulating mutations at a steady rate of two per month—not especially impressive for a virus. These mutations have largely had little effect.
But recently, three distinct versions of the virus seem to have independently converged on some of the same mutations, despite being thousands of miles apart in the United Kingdom, South Africa, and Brazil. (A mutation is a genetic change; a variant is a virus with a specific set of mutations.) The fact that these mutations have popped up not one, not two, but now three times—that we know of—in variants with unusual behavior suggests that they confer an evolutionary advantage to the virus. All three variants seem to be becoming more common. And all three are potentially more transmissible.
“Anytime when you have mutations that come up independently of each other in multiple places, it’s really a sign,” says Vineet Menachery, a coronavirus researcher at the University of Texas Medical Branch. Now scientists are scrambling to figure out if and how these mutations might give the viruses an edge.
It’s still early, and data on the variant in Brazil are particularly sparse. In addition to sharing certain mutations, though, these variants simply have a large number of mutations, some unique to each variant. Gaining a whole suite of mutations quickly should be a very uncommon event. But with the virus so widespread right now, very uncommon events will happen—and will happen more than once. The usual two-per-month mutation rate may undersell how the coronavirus can mutate in unusual situations. “It’s a little bit of a wake-up call,” Kristian Andersen, a microbiologist at Scripps Research, told me.
The role of each individual mutation is still unclear, but a particular mutation in the spike protein called N501Y is noteworthy because all three variants have it. The spike protein is how the coronavirus enters cells, and N501Y is in an especially important region called the receptor-binding domain, which latches on to the cell. An N501Y mutation may make the spike protein stickier, allowing it to bind to and enter cells more readily. Such a virus could become more transmissible. On the plus side, however, the mutation doesn’t seem to affect immunity from vaccines.
Here’s how to read the names of the mutations, by the way: Proteins are made up of building blocks called amino acids. N501Y means that the 501st amino acid was originally an N, which stands for the amino acid asparagine, but has been changed to a Y, which stands for tyrosine.
N501Y is not unique to these three variants, though; it’s been found in a number of sequences around the world. What is unusual about these three variants is that they also have an additional constellation of other mutations in other parts of the virus. A change in a variant’s behavior, such as increased transmissibility, is probably “due to not just one mutation, but multiple mutations,” says Emma Hodcroft, a molecular epidemiologist at the University of Bern. The U.K. variant has more than a dozen other mutations, which have not been scrutinized as much as N501Y. But the variant’s increased transmissibility is looking more certain: It’s growing more prevalent not just in the U.K., but also in Ireland and Denmark, two other countries that regularly sequence large numbers of samples. The CDC recently warned that it’s likely to become the dominant variant in the United States by March.
(Scientists have given all three variants more specific names, but they have not, alas, standardized them yet. The U.K. variant is also known as B.1.1.7, and 20I/501Y.V1, and VOC 202012/01. The South Africa variant is sometimes called B.1.351 or 20C/501Y.V2. The Brazil variant is known as P.1 and 20J/501Y.V3.)
The South Africa and Brazil variants also have a second and third mutation in common in the spike’s receptor-binding domain: E484K and K417. Scientists know a little bit more about the E484K mutation. It switches a negatively charged amino acid for a positively charged one; it’s like flipping a magnet. This likely changes the spike protein’s shape as it is binding to a cell, but this change seems to work in synergy with the N501Y mutation, Andersen said. These mutations, possibly along with others, may make the virus better at binding to cells.
But the South Africa and Brazil variants might have an additional advantage. A recent study suggests that viruses with the E484K mutation might be better at evading antibodies from the blood plasma of recovered C19 patients. Some viruses with this mutation could become a little better at reinfecting people or even infecting vaccinated people.
This one mutation alone is unlikely to render immunity from previous infections or vaccines totally ineffective, though. With current vaccines, “you have more than enough antibody, and even if you cut that amount in half, you still have more than enough antibody to control the virus,” Menachery told me. “If the new variant reduces the efficacy … by 50 percent, you still have a lot of protection there.” Studies are ongoing to figure out exactly how much this mutation affects vaccines, but it does suggest that vaccine makers might need to update their shots if more mutations like E484K accumulate over a period of years. This is already done every year with the flu shot, and the current mRNA C19 vaccines can be updated especially quickly, in as little as six weeks, according to the manufacturers.
Scientists now wonder whether the variants in South Africa and Brazil are spreading precisely because they have this slight advantage in overcoming previous immunity. Both variants were originally found in parts of the countries that have had high levels of C19 infection—especially in Manaus, Brazil, where an especially large proportion of people have already had the virus. (One December study says 76%, which is probably an overestimate, but the region’s high C19 death toll suggests that it indeed had a huge outbreak in 2020.)
The South Africa variant is becoming dominant in the country; the situation in Brazil is less clear because less data exist, but Manaus is currently experiencing another big surge of C19. Menachery said he doesn’t think previous immunity is necessarily a reason for these variants to become more common, especially because South Africa isn’t as close to herd immunity. Better transmissibility is already an advantage.
But others sketched this plausible, though still hypothetical, scenario: The variants may have evolved in immunocompromised patients who were infected with the virus for months. Normally, Hodcroft says, “your immune system is going to town on it. It’s really trying to beat it up.” But immunocompromised patients mount weaker immune responses. “It becomes almost like a training course for how to live with the human immune system,” she says. That may be why these variants have so many new mutations at once, as if a year or two of evolution has been compressed into months. This is probably quite rare, but with tens of millions of infections around the globe, rare things will show up.
A variant could emerge, then, from the training ground of a chronic infection, with mutations that make the virus better at binding to cells and thus more transmissible. This may be what happened with the U.K. variant. It could also emerge slightly more capable of reinfection. This may be what’s happening in Brazil, where there are already two documented cases of reinfection with the new variant. In a place where many people have already been infected with C19, a variant that is just a little better at evading preexisting immunity will have an advantage. These reinfections might not be serious, and they still might not be the norm, but over time, that variant will win out. The coronavirus is in a constant arms race against our immune system. It will keep evolving.
That means our vaccines may need to evolve with it. But the United States is sequencing only a tiny percentage of its C19 cases. (Standard C19 diagnostic tests probe a few regions of the virus genome, but they don’t sequence the whole thing.) “San Diego is one of the places in the country we’re doing well, and we’re sequencing 2 percent of cases. It’s laughable compared to the U.K. and Denmark,” Andersen said. “And we need to change that.” The sequencing data, when they are collected, are fragmented across individual labs all over the country. What the U.S. needs, Andersen said, is a federal mandate for genomic surveillance. That’s the only way for the U.S. to keep abreast of an ever-changing virus.

Source: https://www.theatlantic.com/health/archive/2021/01/coronavirus-evolving-same-mutations-around-world/617721/

5. “It’s Killing Younger People” – New COVID Strain Reportedly Emerging Within Brazilian Amazon

As warnings about the hyper-infectious COVID strains first isolated in the UK and South Africa ring out across the US, Europe and, well, the rest of the world, too, at this point, authorities in Brazil fear they may have a new strain on their hands that’s more infectious, and deadlier, than anything the world has seen previously.
According to a report published by Brazilian outlet Universo Online, a surge in cases and deaths, particularly among younger patients, in the hard-hit Amazonian city of Manaus (situated in northwestern Brazil, on the banks of the River Negro) has drawn the attention of health professionals working on the front lines of the pandemic in the hard-hit Latin American powerhouse.
Several officials with direct knowledge of the situation told UOL that a new “variant” – a mutated strain of the virus – may be responsible for harsher symptoms, and quicker onset times.
But the most alarming shift has been a surge in deaths among younger people, who are dying now in greater numbers than in earlier waves of the outbreak in Manaus, which has long struggled with overburdened health-care resources.
According to Manaus death records from the past 30 days cited by ULO, four out of ten deaths during that time involved patients under the age of 60 in the state.
The UOL analyzed the latest data Transparency Portal of the registry offices. There were 710 deaths in the state (since it may still increase), of which 285 were people under 60 years old – or 40.1% of the total. Before that period, this percentage was 36.5%. “Without a doubt many more young people are dying.
“We are not just talking about a risk group: this is in all age groups, affecting babies, children, teenagers even without comorbidity“, points out the infectologist Silvia Leopoldina, who also works in the state public networks and municipal of Manaus. The doctor says there were changes in the behavior of the disease in the state. “Before, the first symptoms of severity appeared around the tenth day onwards. Now there are patients who, with seven, eight days, are involved in 75% of both lungs.”
“Something very different is happening in Manaus. I don’t know if it is a new strain or if it is something different. But those on the front line are seeing an increase in the severity of the cases,” says infectologist and researcher Noaldo Lucena, who works in popular clinic, home care and public hospitals.
The new infection and death numbers are so severe, he says, they go beyond the already known greater contagiousness of the new variant of the virus.
“Clearly, we are facing an invisible being that is much more pathogenic and transmissible. Today whole families arrive with the symptoms at the same time, before it was one at a time.”
Lucena added that patients in Manaus are also seeing more severe damage to their lungs.
“This year, I have seen 150 more people here at the clinic and 300 more in the public service. I say that less than 2% of them had mild impairment. The rest were over 50%. Some with 70%, 80%, 90%, requiring immediate hospitalization and even ventilatory support,“ he said.
The lung damage is also becoming harder to detect on initial examination.
“You auscultate the patient’s lungs and hear nothing. But when you see the tomographic image, you don’t believe how there is such a huge commitment with so little noticeable clinical repercussion.”
While researchers are still working to confirm exactly what is causing the surge in deaths and severity in Manaus, the biggest fears remain: that new mutations of C19 might be able to pierce through immunity from past infections, and the vaccine.

Source: https://www.zerohedge.com/covid-19/its-killing-younger-people-new-covid-strain-reportedly-emerging-within-brazilian-amazon

6. Previous C19 infection may offer less protection from new variant

Previous infection with the coronavirus may offer less protection against the new variant first identified in South Africa, scientists said on Monday, although they hope that vaccines will still work.
Studies also found that the new variant binds more strongly and readily to human cells. That helps explain why it seems to be spreading around 50% quicker than previous versions, leading South African epidemiologist Salim Abdool Karim said.
The 501Y.V2 variant was identified by South African genomics experts late last year. It has been the main driver of a second wave of national C19 infections, which hit a new daily peak above 21,000 cases earlier this month.
It is one of several new variants found in recent months, including others first discovered in England and Brazil, which scientists worry are hastening the spread of C19.
“Convalescent serum studies suggest natural antibodies are less effective,” Abdool Karim said, introducing the research, “(but) current data suggest the new variant is not more severe.”
British scientists and politicians have expressed concern that vaccines currently being deployed or in development could be less effective against the variant.
Scientists speaking at the virtual panel on Monday said there was not yet a clear answer to that question and that studies were continuing.
“We have reason to be concerned because the virus has found a way to escape from previous antibodies,” Alex Sigal, a virologist at the Africa Health Research Institute, said.
“The world has underestimated this virus. This virus can evolve, it … is adapting to us.”
Earlier, South African researchers said that since vaccines induce a broad immune response it was unlikely that the mutations in the spike protein of the variant would completely negate their effect.
The researchers reiterated that notion on Monday.
“Our immune systems are extraordinarily clever,” Willem Hanekom, one of the team, said. “There may be compensation through other arms of the immune system that allow vaccines to still work”.
The 501Y.V2 variant has spread to nations in Europe, Asia and the Americas, as well as several other African countries, causing some states to impose restrictions on travel to and from South Africa.

Source: https://nypost.com/2021/01/19/previous-covid-19-infection-may-offer-less-protection-from-new-variant/

7. How the novel coronavirus has evolved

As the coronavirus (SARS-CoV-2) swept across the world and killed more than 1.5 million in the past year, it has mutated into several major groups, or strains, as it adapted to its human hosts. Mapping and understanding those changes to the virus is crucial to developing strategies to combat the C19 disease it causes.
Reuters analyzed over 185,000 genome samples from the Global Initiative on Sharing All influenza Data (GISAID), the largest database of novel coronavirus genome sequences in the world, to show how the global dominance of major strains has shifted over time.
The analysis shows there are currently 7 main strains of the virus. The original strain, detected in the Chinese city of Wuhan in December 2019, is the L strain. The virus then mutated into the S strain at the beginning of 2020. That was followed by V and G strains. Strain G mutated yet further into strains GR, GH and GV. Several other infrequent mutations were collectively grouped together as strain O.

“The reason for looking at the genomics is to try and find out where it came from … in terms of trying to map out what we would expect for the pandemic, that information is critical,” South Australia’s chief health officer, Nicola Spurrier, said following an outbreak in the state in early November.
The graphic above shows how the original L strain is almost gone, leaving G strains dominant in the current stage of the pandemic. That’s important because the G strains include one mutation that makes it easier for the spike proteins on SARS-CoV-2 to bind to receptors on human cells, potentially increasing the chances of infection and transmissibility of the virus.
For a closer, graphical look at the mutations, click on the link below.

Source: https://graphics.reuters.com/HEALTH-CORONAVIRUS/EVOLUTION/yxmpjqkdzvr/

D. New Scientific Findings & Research

1. Loss of smell is the best sign of C19

Two international studies confirm that for the majority of patients with respiratory infections who lose the sense of smell, this is due to C19. The disease also often results in both loss of taste and the other senses in the mouth. A researcher from Aarhus University has contributed to the new results.
If you have had C19, then forget about enjoying the smell of freshly made coffee. At any rate, two major international studies document that there is frequently a loss of smell and that this often lasts for a long time in cases of C19.
Alexander Wieck Fjaeldstad, is associate professor in olfaction and gustation at Aarhus University, and is behind the Danish part of the study.
The study shows that the average loss of the sense of smell was 79.7 on a scale from 0-100 – which indicates a large to complete sensory loss, says the researcher. In addition, the studies show that the loss of smell is very probably the best predictor of C19 among patients with symptoms of respiratory diseases.
“This emphasizes how important it is to be aware of this symptom, as it may be the only symptom of the disease,” says Alexander Wieck Fjaeldstad, who also stresses only around half of patients with a loss of smell have gotten their sense of smell back after forty days.
“This differs from the picture we see with other viral infections and causes long-term discomfort for patients, both in relation to food and social contact, while at the same time causing them worry.”
In addition to the loss of the sense of smell, the sense of taste was also significantly reduced, to 69.0 on a scale from 0-100, just as the remaining sense of feeling in the mouth was also reduced, this time to 37.3 on a scale from 0-100.
“While the loss of smell in itself removes the ability to sense the aroma of food, the simultaneous loss of the other senses make it difficult to register what you’re eating. Putting food in your mouth can therefore become a decidedly unpleasant experience,” explains Alexander Wieck Fjaeldstad.
A total of 23 nationalities and over 4,500 C19 patients from all over the world have responded to the researchers’ questionnaire.
“The study is of interest both to patients suffering sensory loss as well as clinicians and researchers who work with diagnostics and following-up on C19. It shows that the loss of smell is specific to C19, which is both relevant in relation to recognising the infection, and because it indicates that the sense of smell is closely linked to how SARS-CoV-2 infects the body.”
Previously, researchers have based the correlation between C19 and the loss of the chemical senses on smaller studies, while these studies collect large amounts of data from countries all over the world.

Source: https://www.eurekalert.org/pub_releases/2021-01/au-los011921.php

2. Surprising New Study Finds That People Who Wear Masks Are More Likely to Become Infected With C19 Than Those Who Don’t

A unique new study suggests that the behavior public officials are now mandating or recommending unequivocally to slow the spread of surging C19 — wearing a face covering — should come with a caveat. If not accompanied by proper public education, the practice could lead to more infections.
The finding is part of a unique study, just published in JMIR Public Health and Surveillance, that was conducted by a team of health economists and public health faculty at the University of Vermont’s Larner College of Medicine in partnership with public health officials for the state of Vermont.
The study combines survey data gathered from adults living in northwestern Vermont with test results that showed whether a subset of them had contracted C19, a dual research approach that few COVID studies have employed. By correlating the two data sets, researchers were able to determine what behaviors and circumstances increased respondents’ risk of becoming sick.
The key risk factor driving transmission of the disease, the study found, was the number of daily contacts participants had with other adults and seniors.
That had relevance for two other findings.
Those who wore masks had more of these daily contacts compared with those who didn’t, and a higher proportion contracted the virus as a result.

Basic human psychology could be at work, said Eline van den Broek-Altenburg, an assistant professor and vice chair for Population Health Science in the Department of Radiology at the Larner College of Medicine and the study’s principal investigator.
“When you wear a mask, you may have a deceptive sense of being protected and have more interactions with other people,” she said.
The public health implications are clear. “Messaging that people need to wear a mask is essential, but insufficient,” she said. “It should go hand in hand with education that masks don’t give you a free pass to see as many people as you want. You still need to strictly limit your contacts.”
Public education messaging should make clear how to wear a mask safely to limit infection, van den Broek-Altenburg added.
The study also found that participants’ living environment determined how many contacts they had and affected their probability of becoming infected. A higher proportion of those living in apartments were infected with the virus compared with those who lived in single-family homes.
“If you live in an apartment, you’re going to see more people on a daily basis than if you live in a single-family home, so you need to be as vigilant about social distancing,” van den Broek-Altenburg said.
The study controlled for profession to prevent essential workers, who by definition have more contacts and are usually required to wear masks, from skewing the results.
“It’s generally known that essential workers are at higher risk, and our study bore that out,” van den Broek-Altenburg said. “We wanted to see what else predicted that people were going to get sick,” she said.

Source: https://scitechdaily.com/surprising-new-study-finds-that-people-who-wear-masks-are-more-likely-to-become-infected-with-covid-19-than-those-who-dont/

3. Saliva could hold clues to how sick you will get from C19

To the known risk factors for developing severe C19—age, male sex, or any of a series of underlying conditions—a new study adds one more: high levels of the virus in your saliva. Standard C19 tests sample the nasal passage. But several new tests look for the coronavirus (SARS-CoV-2) in saliva, and the new work finds a striking correlation between high virus levels there and later hospitalization or death. If the results are confirmed, saliva tests could help doctors prioritize which patients in the early stages of the disease should receive medicines that drive down levels of the virus.
The new work isn’t the first to link the body’s coronavirus load and disease outcome. Several research groups have found a correlation between high viral levels in the nasal passages at the time of a patient’s hospital admission and ultimate disease severity. But other groups have failed to find that same link.
Yale University researchers were among the first, and the university’s hospitals have been using both saliva and NP swab tests. In both cases, labs analyze the samples using quantitative reverse transcription polymerase chain reaction tests, which can detect genetic material from SARS-CoV-2 and quantify the number of viral particles in each milliliter of sample.
Researchers led by Akiko Iwasaki, an immunologist at Yale, compared viral loads in saliva and NP swabs from 154 patients and 109 people without the virus. They divided the patients into groups that had low, medium, and high viral loads as determined by both types of test. Then they compared those results with the severity of symptoms the patients developed later.
They found that patients who developed severe disease, were hospitalized, or died were more likely to have had high virus loads in their saliva tests, but not in their NP swabs. Viral load in both saliva and nasal mucus declined over time in patients who recovered, but not in those who died.
When Iwasaki and her colleagues reviewed patients’ electronic medical records for markers of disease in the blood, they found that high saliva viral loads correlated with high levels of immune signals such as cytokines and chemokines, nonspecific molecules that ramp up in response to viral infections and have been linked to tissue damage.
People with more virus in their saliva also gradually lost certain cells that mount an immune response against viral targets, had lower levels of antibodies targeting the spike protein that the virus uses to enter cells, and were slower to develop the strong immune response needed to knock down the virus in cases where they recovered. The team’s results appeared on 10 January in a preprint that has not been peer reviewed.
Iwasaki and her colleagues argue that saliva may be a better predictor of disease outcome than nasal mucus because the latter comes from the upper respiratory tract, whereas severe disease is associated with damage deep in the lungs. “Saliva may better represent what is going on in the lower respiratory tract,” Iwasaki says, because cilia lining the respiratory tract naturally move mucus up from the lungs into the throat, where it mixes with saliva; coughs have the same effect.
If other research confirms the finding, “it would clear away a lot of the fog” around this disease, Crotty says. Monica Gandhi, an infectious disease expert at the University of California, San Francisco, adds that if saliva tests are predictive, they could help doctors identify patients to treat early with either antibodies to reduce viral load or steroids to tamp down overactive nonspecific immune responses.

Source: https://www.sciencemag.org/news/2021/01/saliva-could-hold-clues-how-sick-you-will-get-covid-19

4. C19 virus triggers antibodies from previous coronavirus infections

The results of a study led by Northern Arizona University and the Translational Genomics Research Institute (TGen), an affiliate of City of Hope, suggest the immune systems of people infected with C19 may rely on antibodies created during infections from earlier coronaviruses to help fight the disease.
C19 isn’t humanity’s first encounter with a coronavirus, so named because of the corona, or crown-like, protein spikes on their surface. Before SARS-CoV-2 — the virus that causes C19 — humans have navigated at least 6 other types of coronaviruses.
The study sought to understand how coronaviruses (CoVs) ignite the human immune system and conduct a deeper dive on the inner workings of the antibody response. The published findings appear today in the journal Cell Reports Medicine.
“Our results suggest that the C19 virus may awaken an antibody response that existed in humans prior to our current pandemic, meaning that we might already have some degree of pre-existing immunity to this virus.” said John Altin, Ph.D., an Assistant Professor in TGen’s infectious disease branch and the study’s senior author.
This knowledge could help researchers design new diagnostics, evaluate the healing powers of convalescent plasma, develop new therapeutic treatments, and — importantly — help design future vaccines or monoclonal antibody therapies capable of protecting against mutations that may occur in the C19 virus.
The researchers used a tool called PepSeq to finely map antibody responses to all human-infecting coronaviruses. PepSeq is a novel technology being developed at TGen and NAU that allows for the construction of highly diverse pools of peptides (short chains of amino acids) bound to DNA tags. When combined with high-throughput sequencing, these PepSeq molecule pools allow for deep interrogation of the antibody response to viruses.
“The data generated using PepSeq allowed for broad characterization of the antibody response in individuals recently infected with SARS-CoV-2 compared with those of individuals exposed only to previous coronaviruses that now are widespread in human populations,” said Jason Ladner, Ph.D., an Assistant Professor at NAU’s Pathogen and Microbiome Institute, which combines the academic genomic research focus of NAU and the translational genomics capacity of TGen. Dr. Ladner is the study’s lead author.
Besides SARS-CoV-2, researchers examined the antibody responses from two other potentially deadly coronaviruses: MERS-CoV, which caused the 2012 outbreak in Saudi Arabia of Middle East Respiratory Syndrome; and SARS-CoV-1, the first pandemic coronavirus that caused the 2003 outbreak in Asia of Severe Acute Respiratory Syndrome. All three are examples of coronaviruses that infect animals, but evolved to make people sick and became new human pathogens.
In addition to characterizing antibodies that recognize SARS-CoV-2, they also examined the antibody responses of four older coronaviruses: alphacoronavirus 229E; alphacoronavirus NL63; betacoronavirus OC43; and betacoronavirus HKU1. These so called “common” coronaviruses are endemic throughout human populations, but usually are not deadly and cause mild upper respiratory infections similar to those of the common cold.
By comparing patterns of reactivity against these different coronaviruses, the researchers demonstrated that SARS-CoV-2 could summon immune system antibodies originally generated in response to past coronavirus infections. This cross-reactivity occurred at two sites in the SARS-CoV-2 Spike protein; the protein on the surface of virus particles that attaches to ACE2 proteins on human cells to facilitate cell entry and infection.
“Our findings highlight sites at which the SARS-CoV-2 response appears to be shaped by previous coronavirus exposures, and which have potential to raise broadly-neutralizing antibodies. We further demonstrate that these cross-reactive antibodies preferentially bind to endemic coronavirus peptides, suggesting that the response to SARS-CoV-2 at these regions may be constrained by previous coronavirus exposure,” said Dr. Altin, adding that more research is needed to understand the implications of these findings.
The findings could help explain the widely varying reactions C19 patients have to the disease; from mild to no symptoms, to severe infections requiring hospitalization, and often resulting in death. It’s also possible that differences in the pre-existing antibody response identified by this study could help to explain some of the difference in how severely C19 disease manifests in old versus young people, who will have different histories of infections with the common coronaviruses.
“Our findings raise the possibility that the nature of an individual’s antibody response to prior endemic coronavirus infection may impact the course of C19 disease,” Dr. Ladner said.

Source: https://www.eurekalert.org/pub_releases/2021-01/ttgr-tsc011821.php

5. C19 reinfections are unusual — but could still help the virus to spread

Most people who catch and recover from C19 are likely to be immune for several months afterwards, a study of more than 20,000 health-care workers in the United Kingdom has found.
The study — called SARS-CoV-2 Immunity and Reinfection Evaluation (SIREN) — concluded that immune responses from past infection reduce the risk of catching the virus again by 83% for at least 5 months.
The data suggest that natural immunity might be as effective as vaccination, she added, at least over the five-month period the study has covered so far.
The data suggest that repeat infections are rare — they occurred in fewer than 1% of about 6,600 participants who had already been ill with C19. But the researchers also found that people who become reinfected can carry high levels of the virus in their nose and throat, even when they do not show symptoms. Such viral loads have been associated with a high risk of transmitting the virus to others, said Hopkins.

Regular screening

Over the 5 months, the team found 44 possible reinfections. In the group of 14,000 participants who had not been previously infected, 318 people tested positive for the virus.
Some of the reinfections are still being evaluated, Hopkins said. All 44 are considered ‘possible’ reinfections, and were classified on the basis of PCR tests combined with screening measures to reduce the risk of re-detecting virus from the initial infection. So far, only 2 of these 44 cases have passed more stringent tests to be classified as ‘probable’. The study did not assess whether symptoms were better or worse during the second infection than during the first, but Hopkins notes that only about 30% of the people with possible reinfections reported any symptoms, compared with 78% of participants with first-time infections.
Investigators are still collecting data; they hope to get a sense of how long immunity lasts and to investigate the effects of a SARS-CoV-2 variant called B.1.1.7 that emerged in 2020 and has rapidly spread across the country. Although there are many reasons to suspect that existing protection should cover new variants, it is possible that immune responses raised against one variant will be less effective against another, says Kassiotis. “It is still an open question.”

Source: https://www.nature.com/articles/d41586-021-00071-6

E. Vaccines & Testing

1. US Vaccine Distribution

Last week, the federal government announced that it was updating its coronavirus (SARS-CoV-2) vaccine distribution plan to release the remaining reserve inventory—as opposed to the previous plan that maintained a stockpile to ensure availability for the second dose.
The announcement was initially met with optimism that state allocations would increase as the US government released the reserved doses; however, multiple news media outlets reported that the federal government actually had relatively few doses in its inventory to distribute to states. The reports were based on statements from senior government officials, including Secretary of Health and Human Services Alex Azar, that the US government did not have any remaining stockpiled vaccines and that it had started distributing the reserved doses in late December, more than a week before the announcement.

Reportedly, some states accelerated plans to expand vaccine eligibility following the announcement, in anticipation of increased supply from the federal government. Notably, Secretary Azar’s announcement that the federal government would release the reserve doses was accompanied by guidance to expand eligibility to all adults aged 65 and older, but without an associated increase in supply, progress in vaccinating such a large portion of the population will proceed slowly.
Pfizer issued a statement indicating that it continues to ship vaccine doses as directed by the US government and that it has “millions more doses sitting in [its] warehouse” awaiting direction from federal officials.
In response to limited vaccine supply from the federal government, New York Governor Andrew Cuomo issued a letter to the Chairman and CEO of Pfizer, Dr. Albert Bourla, requesting to purchase vaccine doses directly from the company. According to the letter, Pfizer does not have any agreement with Operation Warp Speed that would prohibit it from contracting directly with purchasers outside the federal government, but a spokesperson from Pfizer reportedly indicated that it would require authorization from the Department of Health and Human Services to enter into such an agreement. According to CDC data, New York State* has received 9,686 doses per 100,000 population, putting it #15 among US states, and it is #4 in terms of the total number of distributed doses. New York has administered 757,466 of its 1.88 million doses (40%). If New York were to purchase doses directly from Pfizer, it is unclear whether the state would be able to receive any vaccine ahead of Pfizer’s existing contracts, including with the US and other countries.

Source: Johns Hopkins COVID-19 Update

2. New C19 Vaccine: Nanoparticle Immunization Technology Could Protect Against Many Strains of Coronaviruses

The SARS-CoV-2 virus that is causing the C19 pandemic is just one of many different viruses in the coronavirus family. Many of these are circulating in populations of animals like bats and have the potential to “jump” into the human population, just as SARS-CoV-2 did. Researchers in the laboratory of Pamela Björkman, the David Baltimore Professor of Biology and Bioengineering, are working on developing vaccines for a wide range of related coronaviruses, with the aim of preventing future pandemics.
Now, led by graduate student Alex Cohen, a Caltech team has designed a protein-based 60-subunit nanoparticle onto which pieces of up to eight different types of coronavirus have been attached. When injected into mice, this vaccine induces the production of antibodies that react to a variety of different coronaviruses—including similar viruses that were not presented on the nanoparticle.
The research is described in a paper in the journal Science.

Vaccine Induces Cross-Reactive Antibody Response to Multiple Coronaviruses

This new vaccine prototype works by attaching many protein fragments (specifically, receptor-binding domains or RBDs) to an engineered protein-based nanoparticle. The study, in mice, showed that the vaccine induced the production of antibodies that are broadly reactive to a wide range of coronaviruses. RBDs are particularly important for a virus to be able to infect a cell, so antibodies that recognize RBDs are likely more effective at preventing bad infections.

This vaccine platform, called a mosaic nanoparticle, was developed initially by collaborators at the University of Oxford. The nanoparticle is shaped like a cage made up of 60 identical proteins, each of which has a small protein tag that functions like a piece of Velcro. Cohen and his team took fragments of the spike proteins of different coronaviruses (spike proteins play the biggest role in infection) and engineered each to have a protein tag that would bind to those on the cage—the other half of the piece of Velcro. When these viral pieces were mixed together with the nanoparticle cage structure, each virus tag stuck to a tag on the cage, resulting in a nanoparticle presenting spikes representing different coronavirus strains on its surface.
Displaying eight different coronavirus spike fragments (known as receptor-binding domains or RBDs) with this particle platform generated a diverse antibody response, which is an advantage over traditional vaccine methods that present pieces from only a single type of virus. After inoculation, the antibodies subsequently produced by mice were able to react to many different strains of coronavirus. Importantly, the antibodies were reactive to related strains of coronavirus that were not present on the nanoparticle. This suggests that, by presenting the immune system with multiple different coronavirus variants, the immune system learns to recognize common features of coronaviruses and thus could potentially react to a newly emerging coronavirus—not just a SARS-CoV-2 variant—that might cause another pandemic.
Although the team is still studying the mechanism underlying this phenomenon, the results are promising. The next step is to examine whether immunization prevents viral infection and/or infection symptoms in animals making these antibodies.
“If we can show that the immune response induced by our nanoparticle technology indeed protects against illness resulting from infection, then we hope that we could move this technology forward into human clinical trials, though there are a lot of steps that need to happen between now and then,” says Cohen. “We don’t envision that this methodology would replace any existing vaccines, but it’s good to have many tools on hand when facing future emerging viral threats.”
“Unfortunately SARS-CoV-2 is unlikely to be the last coronavirus to cause a pandemic,” says Björkman. “Alex’s results show that it is possible to raise diverse neutralizing antibody responses, even against coronavirus strains that were not represented on the injected nanoparticle. So we are hopeful that this technology could be used to protect against future animal coronaviruses that cross into humans. In addition, the nanoparticles elicit neutralizing responses against SARS-CoV-2, so it could be possible to use them now to protect against C19 as well as other coronaviruses with pandemic potential.”

Source: https://scitechdaily.com/new-covid-19-vaccine-nanoparticle-immunization-technology-could-protect-against-many-strains-of-coronaviruses/

F. Improved & Potential Treatments

1. Researchers test common drugs in quest for treatments for early C19

Little-noticed groups of medical researchers are racing to find treatments for C19 in its early stages, hoping to keep infected people out of the hospital with everyday remedies like antidepressants or vitamins.
They’re pioneering a new approach to medical research — mail-order clinical trials, in which patients can take the medication and monitor its effects without leaving home.
Even though the vast majority of C19 patients ride out the illness at home, most of the research into treatments has focused on those in the hospital, where medical resources are already concentrated and a sense of urgency prevails.
The only outpatient treatments used outside of clinical trials are monoclonal antibodies, lab-made copies of the body’s immune-system fighters. These medications, though in limited supply, have been left largely untapped because of the logistical challenges, including the need for sick people to spend two hours at an infusion center.
Progress has been painfully slow on finding other options. The C19 Early Treatment Fund, which since its founding last spring has doled out $4 million to support such research, expected to have results by October, said Dr. Lisa Danzig, the fund’s chief medical adviser.
Study participants typically must enroll within a few days of testing positive. But people with mild to moderate illness are scattered in the community, may not even be in touch with a doctor — and have been advised not to leave home. “Also, we don’t have a good clearinghouse,” Danzig said. “It’s really hard for people to get information about clinical trials.”
Hundreds of researchers are trying out drugs, supplements, and even over-the-counter medications. The National Institute of Allergy and Infectious Diseases has launched the ACTIV-2 trial, which aims to test several medications at once. Currently it is studying two monoclonal antibody formulations developed to treat C19 and is considering including two antivirals, both repurposed drugs.
Dr. Eric J. Lenze, a psychiatrist and director of the Healthy Mind Lab at Washington University School of Medicine in St. Louis, is studying a surprising candidate for C19 treatment — the antidepressant fluvoxamine, in use since the 1990s and so safe that even an overdose can’t kill you. Lenze has enrolled only about 60 of the needed 1,100 participants so far.
Lenze got interested in fluvoxamine as a weapon against C19 after reading a study showing it could tamp down sepsis in mice. Last year, he recruited a group of 152 COVID-positive patients; he gave fluvoxamine to 80 and a placebo to 72. Not a single one of the patients who took fluvoxamine got sicker during a 15-day period, while six who received a placebo deteriorated, developing shortness of breath or other symptoms.
His research, published in November, was the first placebo-controlled clinical trial to show that medication could prevent severe respiratory symptoms in C19. But it was too small to allow firm conclusions, and Lenze needs to show it works on a larger group.
Lenze is holding out hope that recruitment will be complete by early February (details can be found at https://stopcovidtrial.wustl.edu).
Dr. Melisa Lai-Becker at the Cambridge Health Alliance is also looking at a long-used medication, NAC or N-acetylcysteine, a drug approved in the 1970s that treats acetaminophen overdoses and prevents exacerbations of emphysema.
The idea came to her on a fitful night as the second surge bore down on the Boston area. “I woke up with a start,” she recalled. “All I could think was NAC, NAC.” The drug has been used to treat viral pneumonias, and there’s evidence it can moderate the immune-system overreaction that leads to severe C19.
The study has enrolled 130 of the 200 patients sought (more information here: https://www.nacincovid.info).
Dr. JoAnn Manson, chief of the Division of Preventive Medicine at Brigham and Women’s Hospital, is intrigued by the potential of vitamin D to combat C19, by boosting the immune system early in the infection and tamping down the inflammation that occurs when the immune system goes into overdrive. Her study is looking at whether vitamin D can reduce hospitalization and also whether it can prevent transmission to household contacts of those who are infected.
Open to eligible patients within five days of a positive C19 test, as well as their close contacts, the study plans to enroll 2,700 people. It too uses the trial-by-mail approach, with a finger-prick blood-sampling device. (Details here: www.vividtrial.org).
At the University of Massachusetts Medical School, Dr. Jonathan M. Gerber is studying a product of the human body — blood plasma donated by people who have recovered from C19, known as convalescent plasma. UMass is participating in two national studies led by Johns Hopkins, one testing to see if the plasma can prevent infection in close contacts of C19 patients, and the other seeing if it can prevent worsening of symptoms in those recently infected.
Convalescent plasma is already being used as an inpatient treatment, under an emergency use authorization. Gerber thinks it’s likely to be more effective earlier in the illness, when the immune system may need help fighting off the virus. But the study of outpatients has so far enrolled less than half the target number. (See the article below, ‘Convalescent plasma no benefit to hospital patients’ for more information on this treatment)

Source: https://www.bostonglobe.com/2021/01/14/metro/researchers-test-common-drugs-quest-treatments-early-covid-19/

2. What’s Working in C19 Treatments and What Isn’t

For months, Gilead Sciences Inc.’s remdesivir and the generic steroid dexamethasone have been used on the front lines after being shown to reduce hospital stays and improve recovery speeds. Now, as we learn more about C19, more treatments — including some that at first drew skepticism from physicians and scientists — are proving effective in certain circumstances. Others, such as convalescent plasma, are not. Let’s take a look:

“Toci”

Two arthritis drugs that previously failed in treating C19 — tocilizumab and sarilumab — are now showing a meaningful effect in helping reduce the burden of disease in some patients. It seems that when the drugs are used is key. The latest data comes from a trial involving patients who were treated within 24 hours of needing hospital care in an intensive care unit.
The drugs reduced mortality, suggesting that 7 or 8 lives would be saved for each 100 people treated. The hope is that this data will be corroborated in the U.K.’s much larger and pioneering Recovery trial now underway, with more than 3,000 of the 28,000 and rising participants treated with “toci.” This will provide the most concrete data behind the drug and will potentially enable global approvals beyond Britain.

“Bam-bam”

Bamlanivimab, affectionately known as “bam-bam,” was the first to gain emergency use authorization by the Food and Drug Administration. Both Lilly’s and Regeneron’s treatment have now been cleared for high-risk patients to help prevent hospitalization. One obstacle for adoption of these drugs has been the logistics of administering them — they need to be delivered using specialized infusion equipment.
This difficulty was compounded in bam-bam’s case with a confusing efficacy story and lukewarm comments about it in the Covid-19 treatment guidelines from the National Institutes of Health, resulting in doses piling up on hospital shelves. This situation may be about to change, though, given an early read from a 2,000-patient Mayo Clinic study in which the use of bam-bam was shown to reduce hospitalizations and emergency-room visits by 70%. There are also indications of a reduction in mortality. When data from this study is published, it is likely to drive increased interest in the use of bam-bam, and possibly Regeneron’s antibody treatment, too.

Source: https://www.bloomberg.com/opinion/articles/2021-01-18/what-s-working-in-covid-treatments-like-antibodies-and-plasma

3. ‘Convalescent plasma no benefit to hospital patients’

The results are a blow to researchers and the NHS, which led the drive to collect plasma donations.
This arm of the Recovery trial, which is investigating a number of promising Covid treatments, has now been closed.
Donations of plasma have been temporarily suspended, according to NHS Blood and Transplant.
The treatment involves blood plasma being taken from people who have recovered from the disease – which contains antibodies to coronavirus – and transfused into seriously ill patients.
It was hoped the plasma donation would give the recipient’s struggling immune system a boost to fight off Covid.

‘Value of trials’

But early analysis of 1,873 deaths in a study of 10,400 UK patients shows the treatment made “no significant difference”.
In the group treated with convalescent plasma, 18% of patients died within 28 days – the same figure for the group given standard treatment.
The trial is still investigating other treatments, including tocilizumab, aspirin and an antibody cocktail.
“While the overall result is negative, we need to await the full results before we can understand whether convalescent plasma has any role in particular patient sub-groups,” he said.

Source: https://www.bbc.com/news/health-55681051

4. Encouraging Results on Ivermectin Clinical Trial for Reducing Mild C19

A small pilot study suggests that early administration of ivermectin can reduce viral loads and symptom duration in patients with mild C19, which in turn could help reduce viral transmission. The study, which is part of the SAINT project and has been led by the University of Navarra Clinic and the Barcelona Institute for Global Health (ISGlobal), an institution supported by the “la Caixa” Foundation, warrants further exploration in larger clinical trials. The findings of the pilot study have been published in EClinicalMedicine, a clinical journal published by The Lancet.
We already have two approved C19 vaccines in the European Union, but immunizing enough people worldwide to stop viral spread will require at least two years. Meanwhile, finding drugs that can treat or prevent infections remains a priority. “Many efforts are focusing on developing treatments for C19, but few are addressing how to reduce viral transmission,” affirms study coordinator Carlos Chaccour, researcher at ISGlobal and physician at the University of Navarra Clinic.
In this pilot study performed with patients from the Clinic and in facilities of the University of Navarra, Chaccour and his team evaluated whether the maximal dose of ivermectin recommended in Europe could have an impact on viral transmission when administered within the first days after symptom onset.

Ivermectin is an antiparasitic drug that has been shown to reduce coronavirus (SARS-CoV-2) replication in vitro (in cell lines), albeit at concentrations that exceed those recommended for human use. This, together with preliminary results from a trial in humans that used data of dubious origin and was never peer-reviewed, prompted the use of ivermectin in many Latin-American countries despite the lack of reliable evidence on its efficacy in treating or preventing infection.
The research team gave one single dose of ivermectin or placebo to 24 patients with confirmed infection and mild symptoms, within the first 72 hours after the first symptoms started. Nasal swabs and blood samples were taken at the moment of enrolment and 1, 2 and/or 3 weeks after treatment.
Seven days after treatments, no difference was observed in the percentage of PCR-positive patients (100% of patients were positive in both groups). However, the mean viral load in the ivermectin-treated group was lower (around 3x lower at 4 days and up to 18x lower at 7 days post-treatment), although the difference was not statistically significant. Treated patients also showed a reduced duration of certain symptoms (of 50% for loss of smell and taste and of 30% for cough). All patients developed virus-specific IgG but, again, the mean level of antibodies in the treated group was lower than in the placebo group. “This could be the result of a lower viral load in these patients,” explains Chaccour.
The fact that there was no effect on duration of symptoms or markers associated with inflammation suggests that ivermectin may act through mechanisms that do not involve a possible anti-inflammatory effect. The authors believe it could be interfering with viral entry in the cells, as suggested by another study performed in hamsters at the Pasteur Institute.
“Our findings are in line with those from recent assays conducted in Bangladesh and Argentina,” says Chaccour. “Although our study is small and it is too early to draw conclusions, the trends observed in viral loads, symptom duration and antibody levels are encouraging and warrant further exploration in larger clinical trials with a higher diversity of patients,” he adds.

Source: https://scitechdaily.com/encouraging-results-on-ivermectin-clinical-trial-for-reducing-mild-covid-19/

G. Concerns & Unknowns

1. Depression and stress could dampen efficacy of C19 vaccines

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

Source: https://www.eurekalert.org/pub_releases/2021-01/afps-das011321.php

Also see: C19 vaccine creates incentive to improve our health

2. COVID’s toll on smell and taste

Early in the C19 pandemic, it emerged that many people infected with the coronavirus (SARS-CoV-2) were losing their sense of smell — even without displaying other symptoms. Researchers also discovered that infected people could lose their sense of taste and their ability to detect chemically triggered sensations such as spiciness, called chemesthesis.

How many people with C19 lose their sense of smell?

One review published last June1 compiled data from 8,438 people with C19, and found that 41% had reported experiencing smell loss. In another study, published in August, a team led by researcher Shima T. Moein at the Institute for Research in Fundamental Sciences in Tehran, Iran, administered a smell-identification test to 100 people with C19 in which the subjects sniffed odours and identified them on a multiple-choice basis. 96% of the participants had some olfactory dysfunction, and 18% had total smell loss (otherwise known as anosmia).
Some researchers say that smell loss should be used as a diagnostic test for C19. A study published last October found that self-reported changes in smell or taste were a better marker of the spread of infection than were other indicators tracked by governments, such as arrivals at hospital accident and emergency departments.

Why do people with C19 lose their sensitivity to smells?

Although the mechanisms are not fully understood, there is an emerging consensus that smell loss occurs when the coronavirus infects cells that support neurons in the nose.
When researchers first identified smell loss as a symptom of C19, they were worried that the virus was infecting the odour-sensing neurons in the nose that send signals to the olfactory bulb in the brain — and that the virus could therefore access the brain. However, post-mortem studies4 of people who had had C19 have shown that the virus rarely reaches the brain.
A team led by Sandeep Robert Datta, a neurobiologist at Harvard Medical School in Boston, Massachusetts, has instead found5 that cells that support sensory neurons in the nose — known as sustentacular cells — are probably what the virus is infecting.
Datta and his colleagues zeroed in on sustentacular cells because SARS-CoV-2 attacks by targeting a receptor called ACE2 on the surfaces of cells, and sustentacular cells have many such receptors. Olfactory sensory neurons do not. This suggests that the coronavirus infects the support cells, leaving the neurons vulnerable and deprived of nutrients.

How quickly do the impaired senses return?

For most people, smell, taste and chemesthesis recover within weeks. In a study published last July, 72% of people with C19 who had olfactory dysfunction reported that they recovered their sense of smell after a month, as did 84% of people with taste dysfunction. Claire Hopkins, an ear, nose and throat consultant at Guy’s and St Thomas’ Hospital in London, and her colleagues similarly observed a speedy return of the senses: they followed 202 patients for a month, and found that 49% reported complete recovery over that time, and a further 41% reported an improvement.
But, for others, the symptoms are more serious. Some people whose senses do not return right away improve slowly over a long period — and this can have consequences, says Hopkins. As a person regains their sense of smell, odours often register as unpleasant and different from how they remembered them, a phenomenon called parosmia. “Everything smells rancid” to these people, says Hopkins, and the effect can last for months. This might be because the olfactory sensory neurons are rewiring as they recover, she says.

How does permanently losing the chemical senses affect a person?

Although the condition is not as well studied as the loss of other senses such as vision and hearing, researchers know that the consequences can be severe.
One effect is that it leaves people vulnerable to dangers such as food poisoning and fire. For instance, people with anosmia are less able to detect spoilt foods and smoke. A 2014 study found that people with anosmia were more than twice as likely to experience a hazardous event, such as eating spoilt food, as people without smell loss.

Are treatments available for restoring these senses?

A lack of research means few established treatments exist. But one option is smell training, in which people sniff prescribed odours regularly to relearn them. Hopkins is working with a charity called AbScent in Andover, UK, to get the word out to the public about this training. There is evidence from before the pandemic that it can improve smell function in some people with such impairments, but it doesn’t seem to work for everyone.
Available drugs are even more limited, says Hopkins. But for people in the early stages of C19 infection, when smell loss might be largely due to inflammation of nose cells, steroids might be helpful, according to a preliminary trial carried out by Hopkins’s team.
In longer-term research, Richard Costanzo and Daniel Coelho at Virginia Commonwealth University in Richmond are developing an olfactory implant — a device embedded in the nose that would sense odorant chemicals and send electrical signals to the brain. However, the device is still “many years” from being offered in clinics, says Coelho. In particular, the researchers need to figure out which areas of the brain the implant should stimulate, he adds, so “there’s still some science to work out”.

Source: https://www.nature.com/articles/d41586-021-00055-6

3. Post-COVID lungs worse than the worst smokers’ lungs

A Texas trauma surgeon says it’s rare that X-rays from any of her C19 patients come back without dense scarring. Dr. Brittany Bankhead-Kendall tweeted, “Post-COVID lungs look worse than any type of terrible smoker’s lung we’ve ever seen. And they collapse. And they clot off. And the shortness of breath lingers on… & on… & on.”
“Everyone’s just so worried about the mortality thing and that’s terrible and it’s awful,” she told CBS Dallas-Fort Worth. “But man, for all the survivors and the people who have tested positive this is — it’s going to be a problem.”
Bankhead-Kendall, an assistant professor of surgery with Texas Tech University, in Lubbock, has treated thousands of patients since the pandemic began in March.
She says patients who’ve had C19 symptoms show a severe chest X-ray every time, and those who were asymptomatic show a severe chest X-ray 70% to 80% of the time.
“There are still people who say ‘I’m fine. I don’t have any issues,’ and you pull up their chest X-ray and they absolutely have a bad chest X-ray,” she said.
In X-ray photos of a normal lung, a smoker’s lung and a C19 lung that Bankhead-Kendall shared with CBS Dallas, the healthy lungs are clean with a lot of black, which is mainly air. In the smoker’s lung, white lines are indicative of scarring and congestion, while the COVID lung is filled with white.

X-rays of a normal lung, a smoker’s lung and a COVID patient’s lung.

Dr. Amesh Adalja, an infectious disease expert and senior scholar at Johns Hopkins University Bloomberg School of Public Health, told CBSN that some patients with severe C19 could feel the impact for years to come.
“When someone recovers from pneumonia, whether it’s a bacterial pneumonia or a viral pneumonia, it’s going to take some time for their chest X-rays to improve. Chest X-rays lag your clinical improvement. So you may be better, but your chest X-ray still looks bad,” he said. “And we know that people with C19 can get severe pneumonia, and some of that pneumonia will lead to damage to the lungs that will take time to heal. And some of it may be permanent.”
Bankhead-Kendall said it’s important that if you’re experiencing shortness of breath after your C19 goes away, you stay in touch with your primary care doctor.

Source: https://www.cbsnews.com/news/covid-lungs-scarring-smokers-lungs/

4. Almost 12.5% of readmitted C19 patients die within 5 months

Almost a third of recovered C19 patients in a UK study ended up back in the hospital within five months — and up to one in eight died of complications from the illness, according to a report.
Researchers at the UK’s Leicester University and the Office for National Statistics found that out of 47,780 people discharged from the hospital, 29.4 percent were readmitted within 140 days, the Telegraph reported.
Of the total, 12.3 percent ended up dying, it added.
Respiratory disease was diagnosed in 14,140 of the COVID cases after discharge, with 6,085 of the diagnoses in patients who had no history of respiratory conditions.
The mean age of study participants was 65 years.
Many people who suffer long-lasting effects of the coronavirus develop heart problems, diabetes and chronic liver and kidney conditions, according to the report.
The research also found a higher risk of problems developing in various organs after people younger than 70 and ethnic minorities were discharged from the hospital, according to the Guardian.
“People seem to be going home, getting long-term effects, coming back in and dying. We see nearly 30 percent have been readmitted, and that’s a lot of people. The numbers are so large,” study author Kamlesh Khunti said.
Khunti said the researchers were surprised that many people were readmitted with a new diagnosis, adding that it was important to make sure people were placed on protective therapies, including statins and aspirin.
“We don’t know if it’s because COVID destroyed the beta cells which make insulin and you get Type 1 diabetes, or whether it causes insulin resistance, and you develop Type 2, but we are seeing these surprising new diagnoses of diabetes,” he said.
The study can be read here.

Source: https://nypost.com/2021/01/18/1-in-8-recovered-covid-19-patients-die-within-5-months-study/

H. The Road Back?

1. Population density and transmissibility of virus strains will affect how regions can resume normal life

As a new, apparently more transmissible version of the virus that causes C19 has appeared in several countries, new research finds that the transmissibility of viral strains and the population density of a region will play big roles in how vaccination campaigns can help towns and cities return to more normal activities.
The findings suggest that directing vaccines toward densely populated counties would help to interrupt transmission of the disease. Current vaccination distribution plans don’t take density into account.
Tony Ives at the University of Wisconsin-Madison and Claudio Bozzuto of the independent data research company Wildlife Analysis GmbH studied the spread of C19 in the U.S. at the start of the pandemic, before people changed their behavior to avoid the disease. This let them uncover factors that may affect the transmission of C19 when masking and physical distancing start to wane and behavior once again resembles the pre-pandemic normal.
“We wanted to get at two things: the first was to try and understand what the dynamics were very early in the pandemic. If we need a vaccination program in place that lets people act normally, then we need to understand the state under those conditions,” says Ives, a professor of integrative biology at UW-Madison. “The second was trying to get at a fairly small spatial scale of counties instead of states.”
Parsing out county-by-county data from 39 states through May 23, 2020, Ives and Bozzuto found that the higher a county’s population density, the more readily the coronavirus (SARS-CoV-2) spread from person to person. This county-level spread is ultimately quantified in the basic reproduction number of the virus, a measure of the average number of people an infected person goes on to infect.
The researchers also found compelling evidence that viral strain matters. Ives and Bozzuto saw that the regions hosting a greater proportion of strains containing a mutation called G614 experienced greater viral spread, a finding supported by other research showing that this strain could be transmitted more readily.
While the G614 mutant is unrelated to B.1.1.7, a strain first identified in the United Kingdom that appears to be spreading more easily right now, the new study reflects the importance that viral strain can play in a local area’s overall disease spread.
“We found a clear pattern in the spread rate due to different strains,” says Bozzuto. “Our approach was novel because we went directly to the community level to ask, ‘Can we see any patterns in the data without making assumptions about individual behavior, including strain-related transmissibility and pathogenicity?'”
To track the rate of viral spread, Ives and Bozzuto worked with the number of people who died of C19 last spring. When testing was limited at the beginning of the pandemic, deaths much more accurately tracked C19 transmission. As long as a relatively constant proportion of infected people die from the disease, data on how deaths increase over time will be directly proportional to the overall rate of spread.
Population density predicted a considerable amount of the difference in the rate of viral spread from county to county during the time period the researchers studied. Counties with low or moderate density did not have high rates of infection spread, though lower transmission rates do not necessarily protect a region from eventually seeing high case counts.
Location explained an even greater fraction of the spread in the researchers’ model. Regions within a few hundred miles of one another had similar transmission rates. This regional similarity might have been caused in part by similar public health responses in neighboring counties.
But Ives and Bozzuto also found evidence that regional differences in viral strains explained why neighboring counties looked similar. For example, the low proportion of G614 mutants in the Northwest and Southeast was associated with lower transmission rates.
The researchers investigated several other factors — such as prevalence of obesity and diabetes, socioeconomic status, and political affiliation — and found that none of them contributed significantly to the rate of spread of C19 at the very start of the epidemic. Although these factors may affect how susceptible individuals and populations are to complications from the disease, they didn’t appear to affect the transmission of the virus from person to person.
The new findings were published in the journal Communications Biology on Jan. 5. Ives and Bozzuto say their work can help public health officials decide where vaccines would do the most good.
“Vaccination programs should consider potential spread rate in different areas. The main driver that will be important is density,” says Ives. “From an epidemiological perspective, we would argue that metropolitan areas should be targeted because the level of vaccination or acquired immunity has to be higher than in largely rural areas.”

Source: https://www.eurekalert.org/pub_releases/2021-01/uow-pda011421.php

I. Back to School!?

1. College Campuses Are C19 Superspreaders – Local Campus Outbreaks Rapidly Spread Across the Entire County

COVID-19 Cases Across 30 College Campuses

C19 cases across 30 college campuses. Reported cases for ten high case number, public, and private institutions across the United States since the outbreak of the pandemic.

College campuses are at risk of becoming C19 superspreaders for their entire county, according to a new vast study that shows the striking danger of the first two weeks of school in particular.
Looking at 30 campuses across the nation with the highest amount of reported cases, experts saw that over half of the institutions had spikes — at their peak — which were well above 1,000 coronavirus cases per 100,000 people per week within the first two weeks of class.
In some colleges, one in five students had been infected with the virus by the end of the fall term. Four institutions had over 5,000 cases.
In 17 of the campuses monitored, a new computer model developed by scientists at Stanford University shows outbreaks translated directly into peaks of infection within their home counties.
Out today, the team’s research — published in the peer-reviewed journal Computer Methods in Biomechanics and Biomedical Engineering — crucially shows, however, that tight outbreak management, for example the immediate transition from in person to all online learning, can reduce the peaks within about two weeks.
Lead author Hannah Lu, from Stanford’s Energy Resources Engineering program, says the incidence levels of 1,000 cases per 100,000 people per week — when compared to the first and second waves of the pandemic with peak incidences of 70 to 150 — means colleges are at real risk of developing an extreme incidence of C19.
“Policy makers often use an incidence of 50 C19 cases per 100,000 people per week as a threshold for high risk counties, states, or countries. All 30 institutions in our study exceeded this value, three even by two orders of that magnitude,” she states.
“The number of students who had become infected just throughout the fall is more than twice of the national average since the beginning of the outbreak of 5.3%, with 17.3 million reported cases at a population of 328.2 million.
“At the University of Notre Dame, for instance, all 12,607 students were tested before the beginning of class and only nine had tested positive. Less than two weeks into the term, the seven-day incidence was 3083, with a reproduction number R0 of 3.29.
“However,” she adds, “with around 90 reported deaths nationwide, mainly college employees and not students, the campus-related death rate of 0.02% remains well below the average death rate of C19.”
Members of the research team used advanced modeling, which assesses the real-time epidemiology of the C19 outbreak using an SEIR (susceptible, exposed, infectious, and recovered) model to map how the disease spread across the campuses.
They drew C19 case reports from 30 publicly available college dashboards across the United States throughout the fall of 2020. These institutions were either teaching in person, online or a hybrid of both. They selected colleges for which case numbers are reported on a daily basis and the total cumulative case number exceeded 100.
During this time window, the nationwide number of new cases had dropped below 50,000 per day.
A limitation of this study is that the true on-campus student population was often unreported and had to be approximated by the total fall quarter enrollment. “This likely underestimates of the real maximum incidence and the fraction of on-campus students that have been affected by the virus,” the authors state.
Senior author, Ellen Kuhl, adds: “Strikingly, these local campus outbreaks rapidly spread across the entire county and triggered a peak in new infections in neighboring communities in more than half of the cases.
“It is becoming increasingly clear that these initial college outbreaks are unrelated to the national outbreak dynamics. Instead, they are independent local events driven by campus reopening and inviting students back to campus.
“Our results confirm the widespread fear in early fall that colleges could become the new hot spots of C19 transmission. But, at the same time, college administrators should be applauded for their rapid responses to successfully manage local outbreaks.”
All reported campuses pursued regular surveillance testing, weekly or even twice per week, combined with aggressive test-trace-isolate strategies.
“The majority of colleges and universities were able to rapidly manage their outbreaks and suppress campus-wide infections, while the neighboring communities were less successful in controlling the spread of the virus. As a result, for most institutions, the outbreak dynamics remained manageable throughout the entire fall of 2020 with narrow spikes of less than 300 cases per day,” Lu states.
The team believes that this methodology, in combination with continuing online learning, is the best way to prevent college sites from becoming the major hub of the disease.
“Our study suggests that tight test-trace-isolate strategies, flexible transition to online instruction, and-most importantly-compliance with local regulations will be critical to ensure a safe campus reopening after the winter break,” she added.
Professor Kuhl concludes: “We anticipate that the most important aspect upon campus reopening within the coming weeks will be the human factor. Unfortunately, the fall term has shown that the best of all strategies can become meaningless if people do not follow the recommendations.”

Source: https://scitechdaily.com/college-campuses-are-covid-19-superspreaders-local-campus-outbreaks-rapidly-spread-across-the-entire-county/

2. Colleges Can Prevent 96% of C19 Infections Without Vaccines

The combined effectiveness of three COVID-prevention strategies on college campuses — mask-wearing, social distancing, and routine testing — are as effective in preventing coronavirus infections as the Pfizer and Moderna vaccines approved by the U.S. Food and Drug Administration (FDA), according to a new study co-authored by a Case Western Reserve University researcher.
The research, published in Annals of Internal Medicine, has immediate significance as college semesters are poised to start again — and as the distribution of approved vaccines lags behind goals.
The study found that a combination of just two common measures — distancing and mandatory masks — prevents 87% of campus C19 infections and costs only $170 per infection prevented.
Adding routine lab-based testing to the mix would prevent 92% to 96% of COVID infections. Still, the cost per infection prevented increases substantially, to $2,000 to $17,000 each, depending on test frequency.
As the infection rate continues to rise during the winter, the findings are especially meaningful for institutions of higher learning aiming to strike a balance between in-person and remote instruction, while managing costs to promote safety and reduce transmissions.
“While some measures are highly effective, implementing them is entirely up to each college’s financial situation, which may have already become strained because of the pandemic,” said Pooyan Kazemian, co-senior author of the study and an assistant professor of operations at the Weatherhead School of Management at Case Western Reserve.
“It is clear that two common non-medical strategies are very effective and inexpensive — and allow for some in-person instruction,” said Kazemian. “While it’s true routine testing of the asymptomatic helps catch some infections early and reduce transmissions, they also pose the highest financial and operational burden, even if performed every 14 days.”
Among the study’s other findings:

About three of every four students — and nearly one in six faculty — would become infected over the semester in the absence of all mitigation efforts.
Minimal social distancing policies would only reduce infections by 16% in students.
While closing the campus and switching to online-only education would reduce infections by 63% among students, it would be less effective than opening the campus and implementing a mask-wearing and social distancing policy, which would reduce infections by 87% among students.

Source: https://scitechdaily.com/new-research-finds-colleges-can-prevent-96-of-covid-19-infections-without-vaccines/

3. School risk calculations scrambled by fast-spreading virus strains

A new, more transmissible coronavirus variant has upended efforts to balance the known harm that closed schools cause against the risk that the pandemic virus might spread in classrooms. Studies done before it emerged seemed to point in a hopeful direction: School outbreaks are rare, even when community spread is relatively high, providing schools limit class sizes and require safety measures including masks. And if community spread is low, those safety measures may not be essential, especially among children under the age of 10.
An outbreak of the new variant at a primary school in the Netherlands has undermined that confidence. Tests of 818 teachers, students, and families revealed 123 people—nearly 15%—were infected, just 1 month after the first case was identified at the school, which did not require mask wearing in class. The new variant was responsible for a large fraction of those cases. This week, health officials asked the more than 60,000 residents of the school’s region, north of Rotterdam, to get tested for the virus in an effort to learn how widely it has spread in the community.
In the Netherlands, children attended school full time, with full classes, and were only required to wear masks in hallways and common areas, not at their desks. That may need to change in regions where the new variant is spreading. “We need to be much more vigilant, especially indoors, and put many more safeguards in place,” says Müge Çevik, an infectious disease specialist at the University of St. Andrews. “Given the new variant, all activities will likely be much higher risk.”
But Çevik still thinks schools will be safer than, for example, large groups of adults. “Before the variant, we know primary schools contributed very little to community spread.”
On 16 December, the Netherlands closed all schools as part of a wider shutdown. By then, 40% of students and nearly half the staff at Willibrord reported respiratory symptoms, Fanoy says. Cases also emerged at a second school that shared the building and an associated school at a different campus. In late December, a Willibrord teacher who had been infected died, although officials did not say whether she died of C19 complications.
Despite the Dutch town’s experience, Kanecia Zimmerman, a pediatrician at Duke University who with her colleagues tracked school outbreaks among 100,000 students and staff in North Carolina schools this fall, remains hopeful that with strict measures in place, schools can remain relatively low risk even with the new variant spreading. She and her colleagues found that even in communities with very high transmission—a 14-day incidence of more than 900 cases per 100,000 residents—strict mask requirements and small class sizes (with children attending in person 2 days per week) can keep school outbreaks very rare.

Source: https://www.sciencemag.org/news/2021/01/new-coronavirus-variant-scrambles-school-risk-calculations

4. Everything We Know Now About Schools, Kids, and C19

At a time when kids would normally be starting their spring semester, this post-holiday surge has many state and local officials again grappling with the polarizing issue of in-person education. In hard-hit Southern California, health authorities are calling for a total school shutdown across Los Angeles County. Meanwhile, in New York City, public officials are pushing to keep classrooms open, arguing that as cases in their city spike, schools might actually be the safest place for kids to be.
Last January, as C19 began to sweep across the globe, one of the surprising silver linings of the fast-moving public health crisis was that kids appeared to largely be left out of it. The earliest data from China and Europe showed that the coronavirus infected children only rarely, and mostly caused mild illness when it did. Over the last 12 months, observational analyses of tens of millions of C19 cases and ginned-up surveillance studies have produced much better (though sometimes conflicting) data. Some of the initial science still stands. But much of it has evolved into a more nuanced understanding of how frequently young people pick up, spread, and suffer from SARS-CoV-2. And a year into this pandemic, scientists have finally accumulated enough evidence to say a few things for sure.
The first is that children are, as a whole, less susceptible to the worst outcomes of C19 than people over the age of 18. “They get all the same illnesses as adults, just at a lower rate,” says Lindsay Thompson, a pediatrician and the vice chair for health outcomes and translational research at the University of Florida, who last month wrote a perspective in JAMA Pediatrics summarizing the lessons of the last year. How much lower? In the US, kids are between four and nine times less likely than adults to be hospitalized with C19, and between nine and 16 times less likely to die, according to CDC data. “But it still happens,” says Thompson. “Children have died. Children are dying.”
In April 2020, children under the age of 18 made up just 1.7% of reported coronavirus cases, according to data from the CDC. By August, that figure had shot up to 7.3%. As of January 13, 2021, more than 2 million kids have caught C19, and children comprise 10.8 percent of the nation’s caseload. According to a report released by the CDC on Wednesday, about 12,000 kids were hospitalized with the disease between March 1 and December 12, 2020. During that time, 178 died.
Childhood, however, is not a monolith. Newborns and infants have consistently been found to be at the highest risk, along with kids with underlying health conditions. Then, as kids transform into teenagers, their bodies become more like adults and their social networks expand, putting them more at risk than elementary and middle school students. A pivotal shift appears to happen around the start of puberty. Researchers at the COVID Monitor, a group tracking data from more than 7,000 school districts in the US, recently found that infection rates among high schoolers are triple that of elementary-school-age children.
Age isn’t the only thing that matters. Black and Latino children have disproportionately come down with a constellation of serious heart, gastrointestinal, and kidney complications following bouts with C19. Known as multisystem inflammatory syndrome, or MIS-C, this still-mysterious ailment, while rare, has struck more than 1,600 kids by the CDC’s most recent count.

How easily are kids getting infected, and often are they transmitting the disease to others?

One way researchers have gauged that is to track infections within households where at least one person has tested positive. Two early studies in China found that kids were less likely than the adults in their household to contract the coronavirus. But scientists at the CDC had a hunch that something else was going on. The researchers leading those studies were only swabbing family members if they started to feel sick. Anyone who had been infected but wasn’t showing symptoms would be missed. Moreover, schools in the areas where the families lived were mostly closed. Kids were staying home, reducing their odds of exposure to the virus.
“Back then, there was a ton of discussion about how susceptible kids really were,” says Melissa Rolfes, a CDC epidemiologist with the agency’s C19 response team. “So we set out to get really good data across age spans that wouldn’t be biased by things like symptoms or seeking medical care.”
Rolfes teamed up with researchers in Marshfield, Wisconsin, and Nashville, Tennessee, who’d worked with the CDC in the past on flu surveillance. They quickly stood up a new study focused on finding the coronavirus in kids. It worked like this: If a person tested positive for SARS-CoV-2 and they lived with at least one other person who wasn’t sick, the scientists would try to recruit that whole household for 14 days of daily nasal swabbing and questionnaire answering. That allowed them to capture any viral spread within the household, regardless of who showed symptoms.
What they found between last April and October was stark. People who had the virus spread it to half of their household companions. (In the earlier studies from China, it had been more like 20 to 30%.) And it didn’t matter whether it was a kid or an adult who brought SARS-CoV-2 home, they transmitted it to their family at similar rates. Within households, kids also got infected just as often as adults. But they tended to get less sick than the grown-ups, avoiding fevers and a cough most of the time. “Maybe they’d just have a stuffy nose, or maybe nothing, but when you swabbed them you’d find the virus,” says Rolfes. She realized earlier studies had been overlooking a lot of cases, especially in kids, because they didn’t appear ill. “We were really floored when we saw that data. A secondary infection rate above 50 percent for household contacts was just mind-boggling.”
The study is still ongoing, and Rolfes says those numbers haven’t changed much since October. The takeaway, then, is that symptomatic kids can spread the coronavirus just as easily as symptomatic adults. But Rolfe’s study was limited in one important way: It wasn’t designed to pick up instances when kids without symptoms bring the virus home—or how widely they spread it. To understand that phenomenon, she says, we’ll have to wait a little bit longer.
Still, there have been some super-spreading events at schools and other places where children congregate. The common threads uniting those incidents is that now-rote protective measures like social distancing, mask wearing, and improving ventilation weren’t rigorously enforced. And they happened in places where the virus was already circulating at very high rates.
So, to recap: Kids can catch the coronavirus, like anyone else, although nobody has managed to put a pin in exactly how susceptible they are compared to adults or to younger teenagers, who seem to occupy a middle ground. But they’re less likely to show symptoms, and way less likely to get seriously ill. If they don’t have symptoms, they’re (probably) not going to spread it to a bunch of other people. And kids under 10 are about half as likely to transmit the virus as adults. SARS-CoV-2 can and will spread through schools, but they seem to only become super-spreading hot spots when precautions like masks, distancing, and ventilation are ignored. Schools are always going to be a risk, but one that can be managed—and not being in school is also really bad for kids, for their parents, and for society as a whole. Which is perhaps why the CDC is now recommending that K-12 schools should be both “the last settings to close” and “the first to reopen,” when they can do so safely.

Source: https://www.wired.com/story/everything-we-know-now-about-schools-kids-and-covid-19/

J. Innovation & Technology

1. Using artificial intelligence to spot virus mutations

A big development: Natural-language processing (NLP) algorithms are now able to generate protein sequences and predict virus mutations, including key changes that help the coronavirus evade the immune system. The crucial insight making this possible is that many properties of biological systems can be interpreted in terms of words and sentences.
The latest: In a study just published in Science, a team from MIT demonstrates how they used NLP to predict mutations that allow viruses to avoid being detected by antibodies in the human immune system, a process known as viral immune escape. The basic idea is that the interpretation of a virus by an immune system is analogous to the interpretation of a sentence by a human. The researchers use two different linguistic concepts: grammar and semantics (or meaning). The genetic or evolutionary fitness of a virus—characteristics such as how good it is at infecting a host—can be interpreted in terms of grammatical correctness. A successful, infectious virus is grammatically correct; an unsuccessful one is not.
Why it matters: It’s very early but in theory, knowing what mutations might be coming could make it easier for hospitals and public health authorities to plan ahead. The team says it is now running models on new variants of the coronavirus.
Read the full story.

Source: https://www.technologyreview.com/2021/01/14/1016162/ai-language-nlp-coronavirus-hiv-flu-mutations-antinbodies-immune-vaccines/

2. Smartwatches can help detect C19 days before symptoms appear

Smartwatches and other wearable devices that continuously measure users’ heart rates, skin temperature and other physiological markers can help spot coronavirus infections days before an individual is diagnosed.
Devices like the Apple Watch, Garmin and Fitbit watches can predict whether an individual is positive for C19 even before they are symptomatic or the virus is detectable by tests, according to studies from leading medical and academic institutions, including Mount Sinai Health System in New York and Stanford University in California. Experts say wearable technology could play a vital role in stemming the pandemic and other communicable diseases.

Subtle heartbeat changes

Researchers at Mount Sinai found that the Apple Watch can detect subtle changes in an individual’s heartbeat, which can signal that an individual has the coronavirus, up to seven days before they feel sick or infection is detected through testing. Read the Warrior Watch study.
Specifically, the study analyzed a metric called heart rate variability — the variation in time between each heartbeat — which is also a measure of how well a person’s immune system is working.
“We already knew that heart rate variability markers change as inflammation develops in the body, and Covid is an incredibly inflammatory event,” Hirten told CBS MoneyWatch. “It allows us to predict that people are infected before they know it.”
Individuals with C19 experienced lower heart rate variability, or, in other words, little variation in time between heart beats, in contrast to COVID-negative individuals, the study found.
High heart rate variability does not reflect an elevated heart rate: It indicates that an individual’s nervous system is active, adaptable and more resilient to stress.
“Right now, we rely on people saying they’re sick and not feeling well, but wearing an Apple Watch doesn’t require any active user input and can identify people who might be asymptomatic. It’s a way to better control infectious diseases,” Hirten said.

Source: https://www.cbsnews.com/news/covid-symptoms-smart-watch/

K. Projections & Our (Possible) Future

1. COVID Lockdowns Will Result In 1 Million Excess Deaths Over Next 15 Years

Back in the summer of 2020, a critical discussion almost broke out between progressives on one hand, who were adamant that if “just one life” could be saved with pervasive, widespread economic lockdowns that it was everyone’s imperative to bring the economy to a crawl, and pragmatic, rational thinkers who argued that the economic cost of such lockdowns would end up being far greater than the immediate human cost in terms of lives lost, especially since the impacted lives would be far younger than potential covid vicitms most of whom are in their 70s and 80s. Deutsche Bank credit strategist Jim Reid summarized it best as follows:
- … while the coronavirus has lead to virtually no excess deaths in younger age cohorts, it is the younger strata of society that are the most impact by the economic shutdowns that have resulted in tens of millions of unemployed Millennials.
Reid then argued that since “younger people will be suffering most from the economic impact of C19 for many years to come, we wonder how history will judge the global response.”
Unfortunately as we said at the top, this discussion “almost” happened, although in the end it did not because any time an attempt for rational discourse emerged it would be promptly and violently shouted down by the armies of virtue signalers who were also monetarily incentivized in maintaining the lockdown status quo (such as bankers, pharma and online payment companies, politicians, the media and so on) and who would instantly defer to the “scientists” as the only expert class worth opining on the critical debate of “excess covid deaths now” vs “excess deaths from economic shutdowns later.”
Well, with a roughly one year delay, scientists from Duke, Harvard, and Johns Hopkins finally wrote a paper which may come as a shock to all the virtue-signaling progs out there, because its conclusion is stunning: in a nutshell, the NBER working paper (“The Long-Term Impact Of The C19 Unemployment Shock On life Expectancy And Mortality Rates“) finds that while there have been roughly 400,000 covid-linked deaths so far, the long-term economic implications from covid-related lockdowns are dire, resulting in C19-related unemployment “which is between 2 and 5 times larger than the typical unemployment shock” and resulting in a “3.0% increase in mortality rate and a 0.5% drop in life expectancy over the next 15 years for the overall American population.”
The bottom line, as scientists Bianchi, Bianchi and Song find is that…
- For the overall population, the increase in the death rate following the C19 pandemic implies a staggering 0.89 and 1.37 million excess deaths over the next 15 and 20 years, respectively
That’s bad; where it gets even worse for the world’s progressives is the report’s finding that the “shock will disproportionately affect” women, particularly of Hispanic heritage; African Americans; foreign born individuals; less educated adults and individuals age 16-24.
In short, everyone will be hit by the covid-lockdowns, with blacks, Hispanics and women first, and white men next for a far longer period of time. And, in the process, nearly 1 million excess deaths will take place that wouldn’t have taken place otherwise.
We wonder how those who demanded wholesale economic lockdowns – because that’s the only way to save even one life – will feel now that scientists explicitly state that their preferred policies will lead to nearly a million excess deaths simply from the economic shutdowns.
Here are some more details from the NBER paper:
- While the trade-off between containing the C19 pandemic and economic activity has been analyzed in the short-term, there is currently no analysis regarding the long-term impact of the C19-related economic recession on public health. What is more, most of the papers interested in the relation between the C19 pandemic and economic activity argue, correctly, that lockdowns can save lives at the cost of reducing economic activity, but they do not consider the possibility that severe economic distress might also have important consequences on human well-being. This shortcoming is arguably explained by the fact that current macroeconomic models do not allow for the possibility that economic activity might affect mortality rates of the agents in the economy.
Which merely goes to show just how idiotic macroeconomics as a so-called “science” truly is, because if economists are truly baffled by this “shortcoming”, maybe they should take a look at the millions of small businesses and unemployed service workers to emerge from the covid crisis. Anyway, continuing with the paper:
- Between late March-early April, most U.S. states imposed stay-at-home orders and lockdowns, resulting in widespread shut down of business. Unemployment rate rose from 3.8% in February 2020 to 14.7% in April 2020 with 23.1 million unemployed Americans. Despite a decline to 6.7% in November 2020,the average unemployment rate over the year is comparable with the 10% unemployment rate at the peak of the 2007-2009 Great Recession and it is near the post-World War II historical maximum reached in the early 1980s (10.8%). Importantly, C19 related job losses disproportionately affect women, particularly of Hispanic heritage; African Americans; foreign born individuals; less educated adults and individuals age 16-24. In fact, the unemployment rate underestimates the extent of the economic contraction as many potential workers have abandoned the workforce (especially women).
We fast-forward to the conclusion:
- The long-term effects of the C19 related unemployment surge on the US mortality rate have not been characterized in the literature. Thus, as a last step, we compute an estimate of the excess deaths associated with the C19 unemployment shock. This corresponds to the difference between the number of deaths predicted by the model with and without the unemployment shock observed in 2020. For the overall population, the increase in the death rate following the C19 pandemic implies a staggering 0.89 and 1.37 million excess deaths over the next 15 and 20 years, respectively.
These numbers correspond to 0.24% and 0.37% of the projected US population at the 15- and 20-year horizons, respectively. For African-Americans, we estimate 180 thousand and 270 thousand excess deaths over the next 15 and 20 years, respectively. These numbers correspond to 0.34% and 0.49% of the projected African-American population at the 15- and 20-year horizons, respectively. For Whites, we estimate 0.82 and 1.21 million excess deaths over the next 15 and 20 years, respectively. These numbers correspond to 0.30% and 0.44% of the projected White population at the 15- and 20-year horizons, respectively. These numbers are roughly equally split between men and women.
And the damning piece de resistance is:
- Overall, our results indicate that, based on the historical evidence, the C19 pandemic might have long-lasting consequences on human health through its impact on economic activity. We interpret these results as a strong indication that policymakers should take into consideration the severe, long-run implications of such a large economic recession on people’s lives when deliberating on C19 recovery and containment measures.
- Without any doubt, lockdowns save lives, but they also contribute to the decline in real activity that can have severe consequences on health. Policy-makers should therefore consider combining lockdowns with policy interventions meant to reduce economic distress, guarantee access to health care, and facilitate effective economic reopening under health care policies to limit spread of the coronavirus.
Needless to say, the longer the lockdowns continue, the death toll will only grow bigger across all races and social classes.
And, as we reported last week, a new peer reviewed study out of Stanford has questioned the effectiveness of lockdowns and stay-at-home orders (which it calls NPIs, or non-pharmaceutical interventions) to combat C19. The study’s lead author (an associate professor in the Department of Medicine at Stanford), found that “the study did not find evidence to support that NPIs were effective in preventing the spread” and that “we fail to find strong evidence supporting a role for more restrictive NPIs in the control of COVID in early 2020.”
So, did rushed lockdown policies in response to the pandemic crush economies, and spark mass unemployment and poverty leading to increasing deaths of despair actually achieve anything? The short answer is no…

https://zh-prod-1cc738ca-7d3b-4a72-b792-20bd8d8fa069.storage.googleapis.com/s3fs-public/styles/inline_image_mobile/public/inline-images/California-vs-Florida-covid_0.jpg?itok=BM6Mf7ld

… while the longer answer we now know thanks to the NBER report, is yes: they made the situation for African Americans, Hispanics and women (and yes, even white men) considerably worse for at least the next two decades.
In other words, while lockdowns may not have even led to a tangible improvement in halting the spread of covid, what they will certainly do is lead to hundreds of thousands, perhaps millions, in excess deaths over the next decade.
Which begs the question: now that “respected scientists” have finally quantified the “staggering” excess death toll resulting from covid lockdowns, is it time to finally have the discussion – which nobody has dared to have since about a year ago – about the cost-benefit analysis between widespread economic lockdowns, which will lead over a million early deaths, and locking down the economy every time there is even a modest rebound in covid cases?

https://zh-prod-1cc738ca-7d3b-4a72-b792-20bd8d8fa069.storage.googleapis.com/s3fs-public/styles/inline_image_mobile/public/inline-images/covid%20flowchart_1.jpg?itok=AgvwsCdg

Source: https://www.zerohedge.com/medical/covid-lockdowns-will-result-1-million-excess-deaths-over-next-15-years-scientists-find

L. Lockdowns

1. Peer-Reviewed Study “Did Not Find Evidence” Lockdowns Were Effective In Stopping COVID Spread

A new peer reviewed study out of Stanford is questioning the effectiveness of lockdowns and stay-at-home orders (which it calls NPIs, or non-pharmaceutical interventions) to combat Covid-19. The study’s lead author is an associate professor in the Department of Medicine at Stanford.
“The study did not find evidence to support that NPIs were effective in preventing the spread,” according to Outkick, who published the report.
The study, co-authored by Dr. Eran Bendavid, Professor John P.A. Ioannidis, Christopher Oh, and Jay Bhattacharya, studied the effects of NPIs in 10 different countries, including England, France, Germany and Italy.
And, when all was said and done, it concluded that: “In summary, we fail to find strong evidence supporting a role for more restrictive NPIs in the control of COVID in early 2020.“
In fact, the study found “no clear, significant beneficial effect of more restrictive NPIs on case growth in any country.”
From the study:
- “In the framework of this analysis, there is no evidence that more restrictive non-pharmaceutical interventions (“lockdowns”) contributed substantially to bending the curve of new cases in England, France, Germany, Iran, Italy, the Netherlands, Spain, or the United States in early 2020. By comparing the effectiveness of NPIs on case growth rates in countries that implemented more restrictive measures with those that implemented less restrictive measures, the evidence points away from indicating that more restrictive NPIs provided additional meaningful benefit above and beyond less restrictive NPIs. While modest decreases in daily growth (under 30%) cannot be excluded in a few countries, the possibility of large decreases in daily growth due to more restrictive NPIs is incompatible with the accumulated data.”
The study even looked into the potential of stay-at-home orders facilitating spread of the virus:
- “The direction of the effect size in most scenarios point towards an increase in the case growth rate, though these estimates are only distinguishable from zero in Spain (consistent with non-beneficial effect of lockdowns). Only in Iran do the estimates consistently point in the direction of additional reduction in the growth rate, yet those effects are statistically indistinguishable from zero. While it is hard to draw firm conclusions from these estimates, they are consistent with a recent analysis that identified increase transmission and cases in Hunan, China during the period of stay-at-home orders from increased intra-household density and transmission. In other words, it is possible that stay-at-home orders may facilitate transmission if they increase person-to-person contact where transmission is efficient such as closed spaces.”
- It continues: “We do not question the role of all public health interventions, or of coordinated communications about the epidemic, but we fail to find an additional benefit of stay-at-home orders and business closures. The data cannot fully exclude the possibility of some benefits. However, even if they exist, these benefits may not match the numerous harms of these aggressive measures. More targeted public health interventions that more effectively reduce transmissions may be important for future epidemic control without the harms of highly restrictive measures.”
You can read the full study at https://onlinelibrary.wiley.com/doi/epdf/10.1111/eci.13484.

Source: https://www.zerohedge.com/markets/stanford-peer-reviewed-study-did-not-find-evidence-lockdowns-were-effective-stopping-covid

M. Practical Tips & Other Useful Information

1. What You Need to Know for Traveling in 2021

Like children making lists for Santa, anxious travelers are plotting vacations for the second half of 2021, hoping it will be safe to go by then. Many have already booked. Some are wondering if they’re already too late.
When the calendar changed to a new year, Jack Ezon, co-founder and managing partner of high-end New York travel advisory Embark Beyond, says a deluge of booking requests poured in for summertime trips to Europe. “It’s as if people are asking us for permission to get their lives back,” he says.
A study by home-rental firm Vrbo found 82% of customers already had travel plans for 2021. Even though coronavirus infections and deaths continue to escalate, luxury-travel firm Virtuoso says inquiries about trips started to climb as soon as vaccines were approved last year.
Demand is double-barreled. Many travelers rebooked canceled 2020 trips for dates in 2021 and 2022. In addition, there’s massive pent-up demand for travel.
But travel has changed. It will require more paperwork, preparation and patience. Surprises await those grounded for most of last year.
“It’s no longer get up and go. You have to plan your trip from the moment you walk out the door,” says Peter Vlitas, senior vice president at Internova Travel Group, a network of travel agencies.
Here’s a step-by-step guide to resuming your travel carefully and safely.

1. Book now

Yes, plenty of uncertainty remains. But savvy travelers eager to get moving again have already booked many of the best spots at prime destinations, travel advisers say.
Prices are probably going up as more people get more comfortable with traveling later this year. In many cases, cancellation penalties continue to be waived—though you may end up with a lot of money tied up in credits and vouchers.
“We don’t anticipate seeing many deals for the second half of 2021,” says Keith Waldon, founder and director of Departure Lounge, an Austin, Texas, travel agency.
Another factor: Cancellation policies are likely to get tougher as demand starts to come back, Virtuoso CEO Matthew Upchurch says.

2. Check refund terms

Booking trips for the second half of 2021 isn’t without risk—delays in vaccination distribution or new variants of the virus could prompt lots of shutdowns and closures, and with that trip cancellations. Checking cancellation terms is crucial.
You may be rebooking with a credit from an earlier canceled trip. But what are the terms on your new reservation? If you have to cancel the new reservation, does the credit expire at the original expiration, or a new, longer expiration date? And while your airline, hotel, home rental or cruise may have waived fees and penalties on your first Covid-related cancellation, what about a 2021 cancellation when everyone books knowing the risks?

3. Check health requirements

Assume you’ll have to meet health requirements for different destinations, even on domestic trips. Already many countries and even some U.S. states require negative Covid tests to avoid quarantine. You might even see hotels and airlines require negative test results or even vaccination. (Australia’s Qantas says it may fly only vaccinated passengers on international trips.)
Rules began changing in the U.S. on Tuesday. The Centers for Disease Control and Prevention will require a recent negative test for all passengers arriving from abroad, including U.S. citizens, starting Jan. 26.
In addition, some countries may require proof of health insurance that covers you abroad, so that if you end up in a hospital overseas, the health system there will get paid. Medicare, for example, doesn’t pay for health care outside the U.S. in most cases—you’ll need supplemental insurance or travel insurance that includes health-care coverage.
Stay abreast of changing test and vaccination requirements for international destinations at travel.state.gov. Most airline websites are up-to-date on travel requirements for their destinations. For domestic information, check each state’s website.

4. Research your destination

You need to do more than collect restaurant recommendations. Research local requirements that may differ from national rules in countries. For a few months, Greek islands closed to tourists even when Greece was open, for example. Aspen, Colo., requires a negative C19 test result for anyone 10 or older before hitting the slopes.
Other things to check: Do local authorities allow you to shelter at a hotel or force you to a government-run facility if you become infected? And look at what’s still shut down. Is the resort fully open? Is a tour operator in financial trouble after a year of no business?

5. Use loyalty points

There may be deals to be had using miles and points, because business travel will continue to be depressed, leaving empty first-class and business-class airline seats and hotel suites.
In addition, tickets and hotel reservations booked with points are sometimes easier to refund if plans change, and you don’t have cash tied up in vouchers if things do go wrong.

6. Go with the flow

Schedules are going to change. It’s important to not only avoid close connections and build a cushion into your schedule, but also go into travel this year with a flexible attitude. Travel is going to take longer—there won’t be as many direct flights. And you probably should have a backup plan just in case.
Mike McCormick, former executive director of the Global Business Travel Association, suggests having contact information in your phone for all of your travel providers.
Other smart preparations: Monitor news about your destination for the inevitable changes that will come between booking and travel, and pack extra masks and hand sanitizer, says Mr. McCormick, co-founder of Travel Again, a group backed by travel companies that’s advocating for uniform safety standards.
Masks are not going away. Health checks likely will remain in place for at least a couple of years. Some countries will demand specific information on how to reach you, including hotel reservations and personal cell numbers for contact tracing.
Think carefully about ground transportation. Mr. Waldon suggests avoiding random taxis and guides you haven’t carefully vetted. And expect long lines for rental cars.

7. Slow down and stay simple

This is not the time to be planning whirlwind, multi city tours across a continent. Multiple destinations add potential multiple problems. Mr. Upchurch says even before the pandemic, travelers were shifting to low-and-slow trips, taking time to get to know cultures and communities and make travel more purposeful.
“Disruptions always accelerate trends,” Mr. Upchurch says.

Source: https://www.wsj.com/articles/what-you-need-to-know-for-traveling-in-2021-11610546219

N. Johns Hopkins COVID-19 Update

January 19, 2021

1. Cases & Trends

Overview

The WHO C19 Dashboard reports 93.96 million cases and 2.03 million deaths as of 4am EST on January 15. The global cumulative mortality surpassed 2 million deaths on January 19:

1 death to 250k: 115 days
250k to 500k: 56 days
500k to 750k: 46 days
750k to 1 million: 45 days
1 to 1.25 million: 40 days
1.25 million to 1.5 million: 26 days
1.5 million to 1.75 million: 23 days
1.75 million to 2 million: 20 days

The global weekly incidence decreased for the first time since the week of November 23*. The weekly total of 4.73 million new cases is approximately equal to the week preceding the holidays (4.65 million). Global mortality continues to increase, however, up to 93,882 new deaths, a new record high and an 8.7% increase compared to the previous week.
Our World in Data reports that 41.39 million vaccine doses have been administered globally.

United States

The US CDC reported 23.65 million total cases and 394,495 deaths*. The US is averaging more than 220,000 new cases per day. At this pace, the US could surpass 25 million cumulative cases within the next week. The US could potentially surpass 400,000 cumulative deaths this afternoon—which would include deaths reported on both January 17 and 18.
C19 incidence in the US has declined steadily since January 11, down from 248,367 new cases per day to 221,692, a decrease of nearly 11%. In light of interrupted reporting over the recent holidays, it is difficult to accurately determine the longer-term trend in C19 data. If the US daily incidence is plateauing or peaking, the exact timing of this transition is unclear. The current daily incidence is approximately equal to immediately prior to the Christmas holiday weekend. It is likely that reporting will be delayed to some degree by the Martin Luther King, Jr. Day holiday weekend, but data from this week and next will hopefully provide a better picture of the current US trend. C19 mortality remains high, at 3,344 deaths per day, approximately equal to the record high of 3,357 reported on January 13.
In addition to decreasing daily incidence and initial indications that mortality could be leveling off, current C19 hospitalizations in the US appear to have passed a peak. As we have covered previously, current hospitalizations tend to be more resilient to holiday-related reporting delays than incidence and mortality, so a decreasing trend can provide additional confidence that the US could be passing its third peak. In addition to current hospitalizations, the CDC reported steady decreases in the percentage of emergency department (ED) visits for C19 or COVID-like illness (CLI) since early January, down from a peak of 8.5% on January 3 to 5.8% on January 14. This could be a result of decreased C19 activity or increases in patients seeking care for other conditions.
Based on data published by the COVID Tracking Project, the declines in C19 hospitalizations are evident in all 4 US regions. The Midwest region peaked in late November/early December, and other 3 regions have peaked since the New Year. On a per capita basis, states on the East and West Coasts and in the South are generally reporting more hospitalizations than in the Midwest, Pacific Northwest, and New England. Overall, only 1 US state, North Dakota, is reporting increased C19 hospitalizations over the past 2 weeks, compared to 33 states holding steady (-10% to +10%) and 17 states reporting decreases.
The COVID Exit Strategy website lists 8 states as Severely Constrained in terms of ICU bed availability: New Mexico (96%), Alabama (90%), Georgia (90%), Nevada (89%), Oklahoma (89%), Rhode Island (88%), Mississippi (87%), and California (85%). As with the data described above, these states are generally located on the East and West Coasts and the South. With respect to total hospital beds, no states are listed as Severely Constrained, and only 1 state is listed as Constrained: Rhode Island (89%). Notably, 20 states are listed as Normal for ICU beds, and 25 are Normal for overall hospital beds.
The US CDC reported 31.16 million vaccine doses distributed and 12.28 million doses administered (39.4%), as of January 15. This includes 1.38 million administered in long-term care facilities. In total, 10.60 million people have received at least 1 dose of the vaccine, and 1.61 million have received both doses. In total, 7.15 million doses of the Pfizer/BioNTech vaccine and 5.12 million doses of the Moderna vaccine have been administered nationwide.
The Johns Hopkins CSSE dashboard reported 24.14 million US cases and 399,828 deaths as of 1:30pm EST on January 19.

2. EMERGING VARIANTS

Several SARS-CoV-2 variants with evidence of increased transmissibility continue to raise alarms as they are identified in more countries. Viruses continually mutate, and the SARS-CoV-2 virus has evolved throughout the pandemic. The specific mutations in the recently identified variants of concern—including B.1.1.7, B.1.351, and P.1—are being investigated for increased transmissibility and potentially immune escape.
Researchers from the US CDC C19 Response Team projected that the B.1.1.7 variant would contribute to a rapid growth in cases in the US early in 2021. The B.1.1.7 has been identified in 122 cases in 20 US states, including California and Florida with at least 40 reported cases each. CDC officials projected that the B.1.1.7 variant is likely to become the dominant variant in the US. In order to avoid uncontrolled spread of this variant, health experts encourage individuals to recommit to recommended control measures such as mask wearing, physical distancing, and enhanced hygiene. The CDC also indicated that rapid vaccination, at the level of 1 million doses administered per day, could dramatically decrease spread of C19, including the B.1.1.7 variant.

3. ETHICAL VACCINE DISTRIBUTION

On Monday, WHO Director-General Dr. Tedros Adhanom Ghebreyesus addressed historical inequities in vaccine access and outlined the importance of avoiding such inequities in the context of C19, warning of a “catastrophic moral failure” if SARS-CoV-2 vaccines are not allocated equitably. For example, low- and middle-income countries (LMICs) received vaccines after wealthier countries during the 2009 H1N1 influenza pandemic. And during the C19 pandemic, these countries are once again in line behind high-income countries that were able to arrange the purchase of vaccines directly from manufacturers.
While approximately 39 million doses have been administered across 49 higher-income countries, one “lowest-income country” has been able to administer only 25 total doses. This stark difference underscores the need for the global community to meet its commitments to equitable and ethical distribution of vaccines to ensure the most vulnerable are protected. The WHO COVAX initiative has received numerous pledges to supply vaccine doses for global distribution, but few countries have delivered on those pledges thus far. Further, countries that have made individual agreements with vaccine manufacturers, ostensibly moving their populations higher in the distribution order, are driving up prices and making it more difficult for LMICs to afford the vaccines.

4. EUROPE VACCINE SUPPLY

Pfizer issued a statement on January 15 indicating that it will temporarily decrease the supply of SARS-CoV-2 vaccine to countries in Europe. According to the statement, the reduced supply is part of an effort to scale up production in European facilities. For example, updates to a facility in Belgium are expected to slow production through January 25, but production capacity is expected to increase starting in mid-February. Despite the short-term delays, Pfizer expects to meet its first-quarter commitments and increase its delivery for the second quarter. Reportedly, the announcement was a surprise to some European countries, and several called on EU leadership to pressure Pfizer to meet its original delivery timeline. Reportedly, the production delay could also potentially affect deliveries to Canada, but efforts are underway to mitigate the delays.

5. IVERMECTIN

Ivermectin, an antiparasitic drug with antiviral properties, has shown promise during in vitro studies by inhibiting replication of SARS-CoV-2 in very small concentrations. Observational studies, case series reports, and ecological analyses have also supported this finding. Today, EClinicalMedicine (published by The Lancet) published the first pilot clinical trial testing ivermectin as a treatment of C19. The study used a double-blinded, placebo-controlled design to evaluate ivermectin’s ability to treat C19 disease or mitigate transmission risk. The study included 24 patients, with half (12) receiving a single dose of 400 mcg/kg of ivermectin and the other half (12) receiving a placebo. The treatment was administered within 72 hours of developing a fever or cough. The researchers collected clinical data and nasopharyngeal swabs on Days 4, 7, 14, and 21 post-treatment to assess detectable SARS-CoV-2 RNA by PCR, viral load, symptom severity, and seroconversion. The treatment group had lower viral loads at Days 4 and 7 and lower IgG titers at day 21, but these differences were not statistically significant. Patients in the did have a statistically significant improvement in the time to recover from hyposmia/anosmia—76 patient-days in the treatment group compared to 158 patient-days in the control group.

6. NORWAY DEATHS

Norwegian health authorities are currently investigating the deaths of 23 elderly individuals who received the Pfizer/BioNTech SARS-CoV-2 vaccine to determine if adverse reactions to vaccination could have contributed to the patients’ mortality. The Norwegian Medicines Agency (NOMA) has investigated 13 of the deaths, concluding that some of the common adverse reactions to the vaccine—including fever, nausea, and diarrhea—could have contributed to the deaths. The Paul Ehrlich Institute is investigating 10 deaths reported in individuals who recently received the SARS-CoV-2 vaccine.
Dr. Steinar Madsen, Medical Director for NOMA, told BMJ that there is no certain connection between the vaccine and the patients’ deaths, but it could be possible that common adverse events that are generally mild in younger, healthier individuals could aggravate pre-existing conditions among older, medically frail individuals. The Norwegian Adverse Drug Reaction (ADR) Registry is continually monitoring adverse events related to SARS-CoV-2 vaccination and publishes public weekly reports. The most recent report (January 14) notes that an average of 45 patients in long-term care facilities die each day, and a statement about the deaths indicates that 400 people per week die at long-term care facilities. It is not unexpected that some individuals who get vaccinated will die of unrelated health conditions, and at this point, there is no evidence pointing to a significant increase in the number of deaths following vaccination in Norway.
In response to the reported deaths, The Norwegian Institute of Public Health updated its SARS-CoV-2 vaccination guidance to ask healthcare providers to weigh the risks of potential adverse reactions against the benefits of vaccination when considering vaccination for elderly, medically frail individuals. Norway continues to prioritize long-term care facility residents for vaccination due to their elevated risk of infection and severe disease.