Coronavirus

(The Guardian, May 27, 2020):

French tests show even mild coronavirus illness leads to antibodies -
Study raises hope of immunity even for those without severe symptoms

A medical study in France suggests even mild cases of coronavirus infection, not requiring hospital treatment, produce antibodies in almost all patients, with the body’s defences against the virus increasing during the weeks of recovery. The research, led by a team from the Pasteur Institute, raises hopes that everyone who has had the disease could acquire some degree of immunity, although it is not clear for how long or to what degree.

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(The Jerusalem Post, May 28, 2020):

COVID-19 immunity lasts only six months, reinfection possible - study

Getting re-infected by the novel coronavirus could be possible within six months of recovery, according to a new study published by a team in Amsterdam. If that is the case, then Israel’s hope of testing 1 million Israelis for antibodies to SARS-CoV-2 partially to keep the economy open in any subsequent rounds may be shattered.

A team of 13 researchers from the country located in the Western Netherlands recently uploaded a paper to Medrxiv, an internet site that distributes unpublished manuscripts about health sciences, after monitoring 10 subjects who had contracted at least one of four species of seasonal coronaviruses over a time span of 35 years (1985 to 2020). In “Human coronavirus reinfection dynamics: lessons for SARS‐CoV‐2,” they claim that “an alarmingly short duration of protective immunity to coronaviruses was found… We saw frequent reinfections at 12 months post‐infection and substantial reduction in antibody levels as soon as 6 months …”

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(New York Magazine, May 27, 2020):

Here’s the Latest Good (and Bad) News About the Coronavirus

Coronavirus patients cease to be infectious two weeks after developing symptoms. This was already conventional wisdom. But a new study from Singapore fortifies the consensus by finding that 100 percent of its 73 observed coronavirus sufferers ceased to have a viable virus in their bodies 11 days after the onset of symptoms.

The coronavirus’s mutations don’t appear to have made it more infectious.
Viruses evolve constantly. And SARS-CoV-2 is no exception: According to researchers at University College London (UCL), the novel coronavirus has produced 273 mutations; of these, 31 have become prevalent. One nightmare scenario for SARS-CoV-2 is that it will evolve into something even more lethal and infectious, as the 1918 influenza virus did before its devastating second wave. Fortunately, a new study from UCL indicates that none of the 31 prevalent mutations of the novel coronavirus are more virulent than the original brand.

The evidence that people who contract the coronavirus develop immunity-conferring antibodies is steadily growing. Last week’s roundup included multiple studies indicating that COVID-19 survivors develop neutralizing antibodies and thus face no immediate risk of reinfection (how long such immunity lasts remains unclear). Now, a study of 160 French doctors and nurses who contracted mild cases of COVID-19 finds that 159 possessed neutralizing antibodies 41 days after showing symptoms. This is significant because many have feared that mild cases of COVID-19 might be insufficient to confer immunity.

Herd immunity will take a lot more time and death to achieve than Sweden had hoped. … Things aren’t working out as planned. The Swedish economy has suffered roughly as severe a downturn as that of Denmark. And in recent days, it’s had the highest per-capita coronavirus death rate in Europe. Until last week, defenders of the Swedish strategy could still argue that it might pay off eventually: The policy was never intended to minimize coronavirus deaths in the immediate term, after all. And if keeping things open gets Sweden to herd immunity faster than other countries do, then the strategy could yield an aberrantly high fatality rate in the early months of the pandemic but an exceptionally low one over its full duration. Unfortunately for Sweden - and for anyone hoping America’s reopenings will get us to herd immunity in short order - a recent study of residents in Stockholm found that just 7.3 percent of people in the Swedish city possessed COVID-19 antibodies in late April.

In the developing world, young people are dying from COVID-19 at unprecedented rates. In wealthy countries, COVID-19 deaths have been overwhelmingly concentrated among the old. But as the novel coronavirus gains ground in less prosperous places, fatality rates are rising among the young. … this alarming trend appears more attributable to grotesque international inequalities than to any viral mutation: Due to high levels of extreme poverty and underfunded health systems, many young people who would recover from COVID-19 with proper medical care are dying in the developing world without it.

Even as America reopens, half of its states have uncontrolled coronavirus spread. A study from the Imperial College of London suggests that 24 U.S. states have an R higher than one - meaning that, on average, every person infected with the novel coronavirus gives the bug to at least one other person. Meanwhile, a separate, peer-reviewed study published in Health Affairs indicates that areas of the U.S. that refused to impose social-distancing orders saw 35 times greater spread of the novel coronavirus than those that did implement such orders.

On a global level, the daily count of new coronavirus infections is as high as it’s ever been. Worldwide, the number of new, confirmed coronavirus cases is growing by about 100,000 a day, which is the highest sustained rate of new infections we’ve seen since the pandemic began.

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(New York Times, May 28, 2020):

Coronavirus Pandemic’s Spread Quickens: Live Coverage

“Even as countries move to reopen, the pandemic is growing at a faster pace.”

The coronavirus pandemic’s pace is quickening worldwide, with nearly 700,000 new known infections reported in the last week after the pathogen found greater footholds in Latin America and the Gulf states.

The increases in some countries can be attributed to improved testing programs. In others, though, it appears that the virus has only now arrived with wide scope and fatal force. … Outbreaks have accelerated especially sharply in Argentina, Brazil, Colombia, Mexico and Peru, with caseloads doubling in some countries about every two weeks. On Tuesday, the World Health Organization said it considered the Americas to be the new epicenter of the pandemic. And although much of the Middle East seemed to avert early catastrophe even as the virus ravaged Iran, case counts have lately been swelling in Kuwait, Saudi Arabia, Qatar and the United Arab Emirates.

new studies suggest that even in some of the world’s hardest-hit cities, the vast majority of people remain vulnerable to the virus. Researchers said it is possible that percentage of people who have been infected so far is still in single digits.

In the United States, where the virus death toll has surpassed 100,000, large-scale testing did not happen as the virus spread with ferocity from late January to early March. The result was a lost month, when the world’s richest country - armed with some of the best-trained scientists and infectious disease specialists - missed a chance to contain the virus’s spread. But even countries that have provided ample testing have not escaped second-wave infections.

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Social factors in the USA that would undermine the effectiveness of any vaccine. Some who are immune-compromised (in highest risk groups) may have concerns - as “under” (or “over”) active immune-systems may not respond as will be intended.

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(Associated Press, May 28, 2020):

Expectations for a COVID-19 Vaccine

Twenty percent of Americans anticipate that a COVID-19 vaccine will be available to the public before the end of the year, while 61% expect it during 2021 and only 17% think it will take longer than that.

If a vaccine against coronavirus becomes available to the public, 49% say they plan to get vaccinated, and 20% say they will not. Another 31% are not sure. A 2019 survey conducted for the National Foundation for Infectious Diseases found a similar number, 52%, planned to get vaccinated against the flu that season.

Among all Americans, 79% say that a vaccine is an important criteria for re-opening activities and businesses in their area, including 46% who say it’s essential for re-opening and 33% who say it’s important but not essential. Among those that feel a vaccine is essential for a safe re-opening, 65% would get immunized when a vaccine is available.

Those planning to get the vaccine are doing so primarily to protect themselves and their families. But many also want to protect their community and believe widespread vaccination is necessary for life to go back to normal.

Among the 20% of Americans who say they will not get the vaccine, concern about side effects is overwhelmingly the top reason for avoiding the vaccine:


Source: http://www.apnorc.org/projects/PublishingImages/052620_g3.JPG

(Josh Bloom, ACSH, May 27, 2020):

Put Your Money On A COVID Drug Before A Vaccine

Eerily beyond the grave words from George Carlin about the virus.

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So…

Who all is going? They dont have things like this where I am at… gee… :slight_smile:

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I was on interferon for hep c. Physically I was somewhat okay but what it did to my mind was a whole other story. Aside from the brief suicidal moment the rest of it was like living in a Twilight Zone episode that I’ll never forget. I would have the most disturbing and strange images in “my mind’s eye” (not hallucinations) that wouldn’t go away. I gave it a name, Spikey, because when it first started I saw little black holes in my arm that quickly grew out into long black spikes. Then one day I was looking at my cat and his fur was gone, just skin, and the little black spikes started growing out of his entire body. I had to look away. They said I would be normal again when it was all over. Am I? Long term effects screw with your autoimmune system, for instance. A few years back I developed Grave’s Disease. No hereditary link to my family. I’m in remission now. Hmm, covid or interferon?

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Googling: “graves disease interferon” yields a number of directly related papers. :thinking:

A couple frinds and I were talking about medicines that are on the market that kill / cure diseases and I brought up interferon …My understanding is it pretty brutal but destroys Hep C which until the mid 2000s was thought to be incurable …

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Epidemiologist finds spike of coronavirus cases in those under age 40 -
Dr. Judith Malmgrem published a pre-print report showing nearly 40%
of coronavirus cases after peak in March were in those under 40-years-old.

(May 28, 2020):

A longitudinal cohort analysis of Washington State Department of Health COVID-19 confirmed case age distribution March 1 - April 19 2020 for proportional change over time using chi square tests for significance (N = 13,934).

Results: From March 1st to April 19, 2020 age distribution shifted with a 10% decline in cases age 60 years and older and a 20% increase in age 0-19/20-39 years (chi-square = 223.10, p <.001). Number of cases over the eight-week analysis period were 0-19 years n = 515, 20-39 years n = 4078, 40-59 years n =4788, 60-79 years n = 3221, 80+ years n = 1332.

0-19 years old: 3.696 %

20-39 years old: 29.267 %

40-59 years old: 34.362 %

60-79 years old: 23.116 %

80+ years old: 9.559 %

Source: “COVID-19 Confirmed Case Incidence Age Shift
to Young Persons Age 0-19 and 20-39 Years Over Time:
Washington State March - April 2020

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With things reopening here in US, people seem to be trying to get “back to normal.” I am still hesitant and avoid going out but a few friends and family have stopped by for an occasional visit lately and now I can’t taste my food. I’m somewhat concerned and hoping it’s just vapor’s tongue.
I guess that’s what I get for trying to be polite and inviting them in… :flushed:

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(WIRED, June 1, 2020):

Meet ACE2, the Enzyme at the Center of the Covid-19 Mystery

ACE2, which stands for angiotensin-converting enzyme 2, is a protein that sits on the surface of many types of cells in the human body, including in the heart, gut, lungs, and inside the nose. It’s a key cog in a biochemical pathway that regulates blood pressure, wound healing, and inflammation. ACE2’s amino acids form a grooved pocket, allowing it to snag and chop up a destructive protein called angiotensin II, which drives up blood pressure and damages tissues. But angiotensin II isn’t the only thing that fits in ACE2’s pocket. So does the tip of the mace-like spike proteins that project from SARS-CoV-2, the coronavirus that causes Covid-19. Like a key turning in a latch, the virus gains entry to the cell through ACE2, then hijacks the cell’s protein-making machinery to make copies of itself. An infection begins.

they found that women and men produced similar amounts of ACE2 inside their lung cells. They also couldn’t find any differences between young adults and older ones. Aging didn’t change ACE2 one way or another.

But the smokers were a different story. When they looked at gene expression inside the lungs of smokers versus nonsmokers, they saw a huge spike in ACE2 coming from one particular kind of cell: secretory goblet cells. The job of these mucous-makers is to coat the inside of the respiratory tract, protecting it from any irritants you might breathe in (like say, tar, nicotine, or any of the other 250 harmful chemicals in cigarette smoke). The more people smoked, the more their goblet cells multiplied in an effort to trap these chemicals before they could damage surrounding tissue. Those expanding goblet cell army ranks fueled a surge in ACE2, as Sheltzer and his coauthors described in a study published in “Developmental Cell” in mid-May.

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The referenced research paper:

(Developmental Cell, May 16, 2020):

Cigarette Smoke Exposure and Inflammatory Signaling Increase the Expression of the SARS-CoV-2 Receptor ACE2 in the Respiratory Tract

Highlights:

Lung ACE2 levels do not vary by age or sex,
but smokers exhibit upregulated ACE2

ACE2 is expressed in several lung cell types, including the secretory lineage

Chronic smoking triggers the expansion of ACE2+ secretory cells

ACE2 is also upregulated by viral infections and interferon exposure

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Summary:

The factors mediating fatal SARS-CoV-2 infections are poorly understood. Here, we show that cigarette smoke causes a dose-dependent upregulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 receptor, in rodent and human lungs. Using single-cell sequencing data, we demonstrate that ACE2 is expressed in a subset of secretory cells in the respiratory tract. Chronic smoke exposure triggers the expansion of this cell population and a concomitant increase in ACE2 expression. In contrast, quitting smoking decreases the abundance of these secretory cells and reduces ACE2 levels. Finally, we demonstrate that ACE2 expression is responsive to inflammatory signaling and can be upregulated by viral infections or interferon treatment. Taken together, these results may partially explain why smokers are particularly susceptible to severe SARS-CoV-2 infections. Furthermore, our work identifies ACE2 as an interferon-stimulated gene in lung cells, suggesting that SARS-CoV-2 infections could create positive feedback loops that increase ACE2 levels and facilitate viral dissemination.

(Dana G Smith, Medium, May 28, 2020):

Coronavirus May Be a Blood Vessel Disease, Which Explains Everything -
Many of the infection’s bizarre symptoms have one thing in common

there is now a growing body of evidence to support the theory that the novel coronavirus can infect blood vessels, which could explain not only the high prevalence of blood clots, strokes, and heart attacks, but also provide an answer for the diverse set of head-to-toe symptoms that have emerged.

“If you start to put all of the data together that’s emerging, it turns out that this virus is probably a vasculotropic virus, meaning that it affects the [blood vessels],” says Mandeep Mehra, MD, medical director of the Brigham and Women’s Hospital Heart and Vascular Center.

In a paper published in April in the scientific journal The Lancet , Mehra and a team of scientists discovered that the SARS-CoV-2 virus can infect the endothelial cells that line the inside of blood vessels. Endothelial cells protect the cardiovascular system, and they release proteins that influence everything from blood clotting to the immune response. In the paper, the scientists showed damage to endothelial cells in the lungs, heart, kidneys, liver, and intestines in people with Covid-19.

“The concept that’s emerging is that this is not a respiratory illness alone, this is a respiratory illness to start with, but it is actually a vascular illness that kills people through its involvement of the vasculature,” says Mehra.

A respiratory virus infecting blood cells and circulating through the body is virtually unheard of. Influenza viruses like H1N1 are not known to do this, and the original SARS virus … did not spread past the lung. Other types of viruses, such as Ebola or Dengue, can damage endothelial cells, but they are very different from viruses that typically infect the lungs.

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The paper referenced in article:

(The Lancet, April 20, 2020):

Endothelial cell infection and endotheliitis in COVID-19

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(ACS Chemical Neuroscience, May 7, 2020):

Expression of the SARS-CoV-2 Entry Proteins, ACE2 and TMPRSS2,
in Cells of the Olfactory Epithelium:
Identification of Cell Types and Trends with Age

The COVID-19 pandemic revealed that there is a loss of smell in many patients, including in infected but otherwise asymptomatic individuals. The underlying mechanisms for the olfactory symptoms are unclear. Using a mouse model … the cell surface protein ACE2 and the protease TMPRSS2 are expressed in sustentacular cells of the olfactory epithelium but not, or much less, in most olfactory receptor neurons. These data suggest that sustentacular cells are involved in SARS-CoV-2 virus entry and impairment of the sense of smell in COVID-19 patients. We also show that expression of the entry proteins increases in animals of old age. This may explain, if true also in humans, why individuals of older age are more susceptible to the SARS-CoV-2 infection.

Our results suggest that SARS-CoV-2 virus accumulates in sustentacular cells first and, by interfering with their metabolism, affects the function of olfactory receptor neurons. The damage to these cells caused by the virus may impair smell sensation as is often observed in COVID-19 patients. … An additional important finding of our work is that the murine OE contains a more intense accumulation of ACE2 protein than the respiratory epithelium. If this is true for the human OE, then the OE (and specifically the sustentacular cells) rather than the respiratory epithelium may be most susceptible to SARS-CoV-2 infection, and for this reason it may be the most relevant source of tissues to detect COVID-19 infection in early stages and in asymptomatic carriers.

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(Medical Xpress, June 2, 2020):

Researchers map SARS-CoV-2 infection
in cells of nasal cavity, bronchia, lungs

In a … study published in the journal “Cell”, scientists at the UNC School of Medicine and the UNC Gillings School of Global Public Health have characterized the specific ways in which SARS-CoV-2 - the coronavirus that causes COVID-19 - infects the nasal cavity to a great degree - replicating specific cell types - and infects and replicates progressively less well in cells lower down the respiratory tract, including the lungs.

The findings suggest the virus tends to become firmly established first in the nasal cavity, but in some cases the virus is aspirated into the lungs, where it may cause more serious disease, including potentially fatal pneumonia.

In one set of laboratory experiments, the researchers used different isolates of SARS-CoV-2 to see how efficiently they could infect cultured cells from different parts of the human airway. They found a striking pattern of continuous variation, or gradient, from a relatively high infectivity of SARS-CoV-2 in cells lining the nasal passages, to less infectivity in cells lining the throat and bronchia, to relatively low infectivity in lung cells.

The scientists also found that ACE2 - the cell surface receptor that the virus uses to get into cells - was more abundant on nasal-lining cells and less abundant on the surface of lower airway cells. This difference could explain, at least in part, why upper airway nasal-lining cells were more susceptible to infection.

The referenced paper (May 20, 2020):

SARS-CoV-2 Reverse Genetics Reveals a Variable Infection Gradient
in the Respiratory Tract

(NEJM, May 28, 2020):

Asymptomatic Transmission, the Achilles’ Heel of Current Strategies
to Control Covid-19

A key factor in the transmissibility of Covid-19 is the high level of SARS-CoV-2 shedding in the upper respiratory tract, 1 even among presymptomatic patients, which distinguishes it from SARS-CoV-1, where replication occurs mainly in the lower respiratory tract. 2 Viral loads with SARS-CoV-1, which are associated with symptom onset, peak a median of 5 days later than viral loads with SARS-CoV-2, which makes symptom-based detection of infection more effective in the case of SARS CoV-1. 3 With influenza, persons with asymptomatic disease generally have lower quantitative viral loads in secretions from the upper respiratory tract than from the lower respiratory tract and a shorter duration of viral shedding than persons with symptoms, 4 which decreases the risk of transmission from paucisymptomatic persons (i.e., those with few symptoms).

Asymptomatic transmission of SARS-CoV-2 is the Achilles’ heel of Covid-19 pandemic control through the public health strategies we have currently deployed. Symptom-based screening has utility, but epidemiologic evaluations of Covid-19 outbreaks within skilled nursing facilities such as the one described by Arons et al. strongly demonstrate that our current approaches are inadequate.

Fingers crossed @Mew.

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Sweden’s state epidemiologist Anders Tegnell now says they should have done more, too many died and if they had to do it again, they’d pick another strategy somewhere between what they did and what the rest of the world (I guess the neighboring countries?) did … He maintains that there is a way to handle it without a total lockdown.

Source in Danish: https://www.msn.com/da-dk/nyheder/udland/sveriges-statsepidemiolog-vi-burde-have-gjort-mere-mod-corona/ar-BB14Xetx

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(Science Magazine, June 2, 2020):

Blood vessel attack could trigger coronavirus’ fatal ‘second phase’

The key is direct and indirect damage to the endothelial cells that line the blood vessels, particularly in the lungs, explains Peter Carmeliet, a vascular biologist at the Belgian research institute VIB and co-author of a 21 May paper in Nature Reviews Immunology. By attacking those cells, COVID-19 infection causes vessels to leak and blood to clot. Those changes in turn spark inflammation throughout the body and fuel the acute respiratory distress syndrome (ARDS) responsible for most patient deaths.

This mechanism could explain why the disease pummels some patients who have obesity, diabetes, and cardiovascular conditions: The cells lining their blood vessels are already compromised.

In healthy individuals, endothelial cells help regulate blood pressure, prevent inflammation, and inhibit clotting, in part through the continual production of nitric oxide (NO); they also serve as gatekeepers for molecules passing in and out of the bloodstream. When injured, they send out a complex array of signals to immune cells and clotting factors, which rush to repair the site.

When SARS-CoV-2 enters the lungs, it invades cells in the air sacs that transfer oxygen to the blood. Surrounding those sacs are capillaries lined like bricks with endothelial cells. The virus directly invades some of those cells; others become “activated,” likely in response to signals from the invading virus and other damaged cells. Some infected cells likely commit suicide. “It’s not a quiet death where the cell just dies,” Mangalmurti says. “All the contents leak out.”

Carmeliet and colleagues suggest damage and other changes in the activated cells trigger vascular leakage, flooding the air sacs with fluid, a hallmark of ARDS. White blood cells swarm to the lungs and NO production likely plummets. Together with the activated endothelial cells, the immune cells release a host of signaling molecules, including interleukins, which raise local blood pressure and weaken cell junctions. Damage to endothelial cells exposes the membrane underneath them.

That exposed membrane in turn triggers uncontrolled clotting. The endothelial and immune cells add fuel to the fire, recruiting additional clotting factors and platelets, which help form clots. Those clots degrade into the key biomarker D-dimer, creating sky-high levels that alert clinicians to patients in trouble. Eventually, such clotting spreads throughout the body, blocking the blood supply within vital organs.

These chain reactions culminate in a final, destructive phase of inflammation. Like clotting, inflammation is an essential defense, sending a diverse army of cells and messenger molecules called cytokines to fight invaders and mop up the debris of battle. But in COVID-19, this reaction spirals out of control in a deadly cytokine storm and plunges patients’ bodies into shock.

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(Ars Technica, June 1, 2020):

SARS-CoV-2 looks like a hybrid of viruses from two different species -
Pieces of several genomes recombined to produce
the pandemic-causing pathogen.

a US-based research team has done a detailed analysis of a large collection of viral genomes, and it finds that evolution pieced together the virus from multiple parts - most from bats, but with a key contribution from pangolins.

How do pieces of virus from different species end up being mashed together? The underlying biology is a uniquely viral twist on a common biological process: recombination.

the research team started with a collection of 43 different coronaviruses from a variety of species, including humans, bats, and the pangolin sequences known to be similar to SARS-CoV-2.

The basic genome analysis confirmed that SARS-CoV-2 is most closely related to a number of viruses that had been isolated from bats. But different areas of the virus were more or less related to different bat viruses. In other words, you’d see a long stretch of RNA that’s most similar to one virus from bats, but it would then switch suddenly to look most similar to a different bat virus. This sort of pattern is exactly what you’d expect from recombination, where the switch between two different molecules would cause a sudden change in the sequence at the point where the exchange took place.

there was a notable exception to this mixing of bat viruses: the spike protein that sits on the virus’s surface and latches on to human cells. Here, the researchers found exactly what the earlier studies had suggested: a key stretch of the spike protein, the one that determines which proteins on human cells it interacts with, came from a pangolin version of the virus through recombination. In other words, both of the ideas from earlier work were right. SARS-CoV-2 is most closely related to bat viruses and most closely related to pangolin viruses. It just depends on where in the genome you look. It’s looking likely that the pangolin sequence is essential for the virus’s ability to target humans.

rumors about this being an escaped weapons experiment make little sense in terms of what the genome sequences tell us about biology.

The authors find evidence that the viruses from different species may experience distinct selective pressure, which isn’t really surprising. But that also can produce difficult-to-predict results when those viruses hop to a new species - and the difficulty will rise if they then exchange information with other viruses native to that species.

Summing this up, there seem to be myriad coronaviruses out there (including plenty we don’t know about), and some species are serving as labs in which new genetic combinations are created. And, right now, we only have a very partial window into the sort of potential out there in species that have frequent contacts with humans. And some research cited by the authors suggests that humans have been exposed to at least some of these viruses (based on antibodies to them) - fortunately without a major outbreak occurring.

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I read that Darwin did not anticipate Horizontal Gene Transfer, and its seems that perhaps his considerations may also have not anticipated Genetic Recombination:

Recombination
Recombination involves the exchange of genetic material between two related viruses during coinfection of a host cell.

Recombination by Independent Assortment
Recombination by independent assortment can occur among viruses with segmented genomes. Genes that reside on different pieces of nucleic acid are randomly assorted. This can result in the generation of viruses with new antigenic determinants and new host ranges. Development of viruses with new antigenic determinants through independent assortment is called antigenic shift.

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Viruses are in a perpetual arm race with their hosts. Camouflage is a common strategy viruses use to escape to the immune system (either innate or adaptive) of their hosts. This generally translates in a propensity to develop replication strategies that are, at different extents, prone to the insertion of mutations in their genome. Accumulation of mutations is nevertheless limited by the need to maintain viability and its own genetic identity. Keeping subtle equilibrium between these two contrasting forces is vital for viruses, it often influences their pathogenic potential, and can be at the origin of outbreaks of infection of relevance for public health.

Recombination is an important source of genetic variability in viruses, particularly for viruses possessing an RNA genome. The remarkable power of recombination resides in its ability, in a single infectious cycle, to generate new combinations of mutations. This is important at two regards: one is that recombination does not generate new mutations but reshuffles pre-existing ones, whose compatibility with viral survival has already been established. This is expected to increase the probability of having a viable recombinant progeny.

On the other hand, the fact that, in general, several mutations are simultaneously introduced through the recombination process, is expected to favour the opposite outcome: that a high proportion of recombinant products will not be viable. Finally, recombination in concert with natural selection, can be responsible of combining advantageous mutations, as well as removing deleterious ones, by far the most abundant type of mutations found in nature.

For many viruses the generation of recombinant variants has been associated to important moments in the processes of adaptation, gain of pathogenic potential or increased spreading.

Source: https://www.mdpi.com/journal/viruses/special_issues/recomb-vir

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Viral Genome Evolution information:

https://viralzone.expasy.org/4136

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(The Lancet, June 1, 2020):

Physical distancing, face masks, and eye protection
to prevent person-to-person transmission of SARS-CoV-2 and COVID-19:
a systematic review and meta-analysis

The findings of this systematic review of 172 studies (44 comparative studies; n=25697 patients) on COVID-19, SARS, and MERS provide the best available evidence that current policies of at least 1 m physical distancing are associated with a large reduction in infection, and distances of 2 m might be more effective. These data also suggest that wearing face masks protects people (both health care workers and the general public) against infection by these coronaviruses, and that eye protection could confer additional benefit. However, none of these interventions afforded complete protection from infection, and their optimum role might need risk assessment and several contextual considerations.

In between study and within-study comparisons, we noted a larger effect of N95 or similar respirators compared with other masks. This finding is inconsistent with conclusions of a review of four randomised trials, in which low certainty of evidence for no larger effect was suggested. However, in that review, the CIs were wide so a meaningful protective effect could not be excluded. We harmonised these findings with Bayesian approaches, using indirect data from randomised trials to inform posterior estimates. Despite this step, our findings continued to support the ideas not only that masks in general are associated with a large reduction in risk of infection from SARS-CoV-2, SARS-CoV, and MERS-CoV but also that N95 or similar respirators might be associated with a larger degree of protection from viral infection than disposable medical masks or reusable multilayer (12–16-layer) cotton masks. Nevertheless, in view of the limitations of these data, we did not rate the certainty of effect as high.

The use of face masks was protective for both healthcare workers and people in the community exposed to infection, with both the frequentist and Bayesian analyses lending support to face mask use irrespective of setting. Our unadjusted analyses might, at first impression, suggest use of face masks in the community setting to be less effective than in the health-care setting, but after accounting for differential N95 respirator use between health-care and non-health-care settings, we did not detect any striking differences in effectiveness of face mask use between settings. …

Physical distancing of at least 1 m is strongly associated with protection, but distances of up to 2 m might be more effective. Although direct evidence is
limited, the optimum use of face masks, in particular N95 or similar respirators in health-care settings and 12–16-layer cotton or surgical masks in the community, could depend on contextual factors.

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