The biology of coronavirus COVID-19 - including research and treatments

Hmm, now, where have I heard this before?

Some covid survivors develop autoantibodies that attack healthy cells

http://www.msn.com/en-gb/health/med...lthy-cells/ar-BB1auwha?li=AAnZ9Ug&ocid=ASUDHP

 

I'm sorry that I haven't been following things very well lately but is there scope for an S4ME response to this? For the research that we wished people had done when we'd got sick?

Covid is quite possibly a mass-ME event. The rest of us got picked off one by one, mostly, over the years, making our epidemiology and our commonalities invisible. This awful Covid thing seems a big opportunity to prevent a lot of future suffering, with the right research.

 

Not sure this is the right thread - article on how aerosol and droplets in different social gatherings and scenarios.

A room, a bar and a classroom: how the coronavirus is spread through the air

The risk of contagion is highest in indoor spaces but can be reduced by applying all available measures to combat infection via aerosols. Here is an overview of the likelihood of infection in three everyday scenarios, based on the safety measures used and the length of exposure

 

This says 'RFI open until 12/7/20'. Is it too late to propose things?

Wondering what research you think should be done now in what is probably a mass-ME-provoking event, @Jonathan Edwards?

 

Inverse has an article on how COVID-19 affects the brain. What strikes me is how little expert neurologists feel certain about. What they do say is that there appear to be some neurological problems lasting a year, which is hard to document, considering the length of this crisis. (I don't doubt this will be true, just wonder where to get evidence at this time.)

This is not to say that existing research indicates no such effects, quite the contrary. See also this study from Wuhan, and this recent study by the NIH.

What we need is a better understanding of neurological effects not just of this virus, but also the immune response to it. This is a big problem. We have evidence in other situations that immune response alone can trigger dramatic neurological effects. (I recall a case in which a patient who received a bone-marrow transplant became hopelessly schizophrenic, like the donor. Because this was considered a "mental illness" nobody had expected this physical change to transmit the illness.)

Neurological damage tends to produce long-term problems which are hard to correct, as in MS or myasthenia gravis, so it would make economic sense to examine immune triggers of these conditions. Unfortunately, we are still far from understanding even the immune responses which are currently protecting many individuals from the most obvious effects of infection. The debate in this thread about the significance of antibody levels is an example. The special immunological status of the CNS makes the problem even more difficult.

A rational response to the problem would be to launch an extensive research program which would also address many problems familiar to those on this forum. Unfortunately, rational responses seem to be in the minority at present.

 

What's the hold-up on the widespread provision of antibody tests? Is it a lack of some raw material, or manufacturing capacity, or what?

 

Merged thread

The New York Times has ran a story on Oct 30th (it's behind a paywall) about a new study in regards to Covid 'long haulers'. Below is the text of the NYT article.....



Some Covid Survivors Have Antibodies That Attack the Body, not Virus

...

The results were reported Friday on the preprint server MedRxiv, and have not yet been published in a scientific journal. But other experts said the researchers who carried out the study are known for their careful, meticulous work, and that the findings are not unexpected because other viral illnesses also trigger autoantibodies.

“I’m not surprised, but it’s interesting to see that it’s really happening,” said Akiko Iwasaki, an immunologist at Yale University. “It’s possible that even moderate to mild disease may induce this kind of antibody response.”

...

Viral infections cause infected human cells to die. Sometimes the cells die a quiet death — but sometimes, and especially in the throes of severe infection, they can blow up, strewing their innards. When that happens, DNA, normally cloistered in coiled bundles inside the nucleus, is suddenly scattered and visible.

In the typical response to a virus, cells known as B immune cells make antibodies that recognize pieces of viral RNA from the virus and lock onto them.

But in conditions like lupus, some B cells never learn to do this and instead produce autoantibodies that glom onto DNA debris from dead human cells, mistaking them for intruders. Something similar may be happening in patients with Covid-19, the research suggests.

“Anytime you have that combination of inflammation and cell death, there is the potential for autoimmune disease and autoantibodies, more importantly, to emerge,” said Marion Pepper, an immunologist at the University of Washington in Seattle.

Dr. Woodruff and his colleagues reported earlier this month that some people with severe Covid-19 also have such unrefined B immune cells. The finding prompted them to explore whether those B cells make autoantibodies.

In the new study, the researchers looked at 52 patients within the Emory health care system in Atlanta who were classified as having either severe or critical Covid-19, but who had no history of autoimmune disorders.

They found autoantibodies that recognize DNA in nearly half of the patients. They also found antibodies against a protein called rheumatoid factor and others that help with blood clotting. Among the top half of the most seriously ill patients, more than 70 percent had autoantibodies against one of the targets tested, Dr. Woodruff said.

“It’s not just that these patients have an autoimmune-like immune response,” he said. “It’s that those immune responses are coupled with actual true testable clinical auto-reactivities.”

Some of the autoantibodies the researchers identified are associated with blood flow problems, noted Ann Marshak-Rothstein, an immunologist and lupus expert at the University of Massachusetts, Worcester.

“It’s very possible that some of the coagulation issues that you see in Covid-19 patients are being driven by these kinds of immune complexes,” she said.

If the autoantibodies do turn out to be long-lasting, she said, they may result in persistent, even lifelong, problems for Covid-19 survivors.

“You never really cure lupus — they have flares, and they get better and they have flares again,” she said. “And that may have something to do with autoantibody memory.”

Dr. Marshak-Rothstein, Dr. Iwasaki and dozens of other teams are closely studying the immune response to the coronavirus. Given the ease of testing for autoantibodies, it may soon become clear whether the antibodies were identified only because the researchers went looking for them, or whether they represent a more permanent alteration of the immune system.

“It’s not clear to me what it all means at this point,” Dr. Pepper said. “It’s going to take a little bit of time to understand if this is something that’s going to lead to downstream pathology.”


link to the study..... https://www.medrxiv.org/content/10.1101/2020.10.21.20216192v2

link to the NYT article.... https://www.nytimes.com./2020/10/27...mmunity.html?smtyp=cur&smid=tw-nytimesscience

 

I would agree with that.

 

This may get outsized attention, not just because it's in the New York Times, but also because the lead author is from Emory University, which is literally across the street from the CDC.

As I recall, the CDC's Dr. Reeves collaborated with Emory University's Department of Psychiatry and Behavioral Sciences in his attempts to find a psychological underpinning for CFS.

 

Algorithm spots 'Covid cough' inaudible to humans
https://www.bbc.com/news/technology-54780460

 

The role of immune response in COVID-19 has been important, and misunderstanding of immune response by medical doctors, let alone the general public, is behind a great deal of confusion. The New Yorker magazine has a nice non-specialist survey of the place of this pandemic in the history of immunology. This virus is remarkably skilled in exploiting immune defenses, not just of humans, but also of other mammals. I'll offer a link in the hope that it will help others to find this material, even though my access comes via a subscription. The title is How Coronavirus Hacks the Immune System.

What this reveals is very similar to the abnormal immune responses most of us experienced at onset of our ME/CFS. Approaching this with common misunderstandings will lead to predictable failures. We need research on the entire immune system as a functioning system, not a random collection of parts, and on the signalling that controls it.

A more easily accessible article from Medical Xpress covers research on the role of superspreader individuals in the epidemic. They report that most spread comes from those who are far from the mean, out in the "fat tail" of the distribution. This means the distribution is far from a "normal distribution". Identifying such individuals could have an outsized effect on containing the pandemic.

 

Researchers find autoantibodies that may be responsible for the blood clotting seen in some COVID-19 patients. Half of the hospitalized patients in the study showed the presence of these autoantibodies at some point.

ETA: This seems to be a different autoantibody study from the one posted above by @TrixieStix

 

Has this possible study been mentioned - the COVID Human Genetic Effort? It sounds like the sort of thing we would all have wished to have had when we got sick with ME.

https://www.nature.com/articles/d41586-020-02598-6

 

This is more of a narrative than a reporting of science (as is the fasion in the New Yorker)

Some parts are clearly nonsense (the talk about cytokine storms and mention of interferons as if they aren't cytokines).

Interestingly enough, the interferon inhibition was already known from research on other coronaviruses, particularly SARS-1. It wasn't so much discovered as simply confirmed in SARS-2. This is also why so many research groups were studying this angle, early on in the pandemic timeline.

The inhibition of an inflammatory response through interferon inhibition is why symptoms can be relatively mild despite a relatively strong viral load, until the viral load gets so high that things get out of control quickly (in severe cases) and there is a rapid build up of immune complexes that are unable to be cleared fast enough - which also seems to drive a feedback loop leading to sensitisation of immune responses against bystanders (such as the aPL antibodies mentioned in a post above), or even the anti-interferon antibodies mentioned a little while ago. It is the lack of clearance of the immune complexes that leads to inflammation and the severe clotting and organ damage.

 

A little concerning regarding vaccines:

More and more mink farms in Denmark are getting infected by corona. It's unclear how the virus is spreading between farms but one suspect is gulls carrying it on their feet (they don't seem to get infected themselves). Up until now infected and neighbouring farms had to kill all their animals.

Now they've found a mutation of the virus in mink which appears to be sufficiently different from other circulating strains that it could limit the effectiveness of a vaccine due to "decreased sensitivity to antibodies". The mutation has spread to humans. So now all mink in Denmark are going to be killed, about 12 million.

The article doesn't give any more specific info than the above summary - it's breaking news - but for anyone interested here's the link:

https://www.dr.dk/nyheder/indland/alle-danske-mink-skal-aflives-af-frygt-virusmutation (Danish)

 

I haven't checked the link but (as a lay person) this seems like a big deal i.e. coronavirus "jumping" from humans to mink and vice versa.

 

I looked briefly online after I posted this. As many of you know this story has been around since the summer i.e. in Spain mink farmers found their animals were sick (coronavirus) and the farmers also developed coronavirus - who caught it from whom isn't clear.
So far it seems that nobody is saying this definitely is a big deal; however, concerns re the effectiveness of the current vaccines are worrying.

Seems to highlight @Jonathan Edwards point i.e. eradicate this virus if you possibly can - at least aim to. The longer it's around/the more people (or animals) infected then the more likely we are to see mutations.

 

Yes, I think this Danish mink thing is highly significant. The perpetual cycle of new flu strains is probably due to a reservoir in Chinese animal stock, maybe ducks. Having a reservoir of millions of animals to allow new mutations to be selected and reintroduced to humans is about the worst possible strategy. I think that there is a very real chance that over the next few months a much more lethal strain will appear.

 

I actually felt quite scared when i read about it this morning, scared of losing people i love. Do you think it will be possible to contain it? or are we basically buggered?

BBC story for anyone interested https://www.bbc.co.uk/news/world-europe-54833459

 

It is perfectly possible to contain the virus. We did it in February but blew it. We nearly did it again in June and blew it. The Australians have done it despite big local outbreaks. It just requires doing the job properly, like in Thailand or China.

In fact, if there is a deadlier strain I suspect eradication will come quicker. The real problem with this virus is that it is dangerous but not so dangerous that everyone can see how dangerous it is. If it were Sars-1 we would have cleared it by now, because the alternative would have been unthinkable.