News Article: "Researchers are closing in on long covid"

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This article published Apr 29th, 2021 has a clear overview of Long-COVID causative theories to date.

https://www.economist.com/science-and-technology/2021/04/29/researchers-are-closing-in-on-long-covid

The first:
Based on these patterns of symptoms, and various laboratory tests of long-covid patients, doctors are focusing on three possible biological explanations. One is that long covid is a persistent viral infection. A second is that it is an autoimmune disorder. The third is that it is a consequence of tissue damage caused by inflammation during the initial, acute infection.

According to the first of these hypotheses, some patients never clear the virus completely. They are not infectious, says Dr Nath, so it could be that they harbour some altered form of the pathogen which is not replicating and is thus undetectable by the standard test for sars-cov-2, but is nevertheless making some viral product that their bodies are trying to fight off. This sort of thing is known to occur with other viruses, including measles, dengue and Ebola. rna viruses, of which sars-cov-2 is an example, are particularly prone to this phenomenon, says Dr Nath.
M
The second:
The second hypothesised mechanism for long covid, that it is an autoimmune disease, holds that the virus, though gone, has caused something to go awry with the immune system—which now attacks some of the body’s own tissues. A growing body of evidence backs this idea, too....

Some of those suffering from long covid have badly behaving macrophages, the cells responsible for detecting and engulfing harmful invaders. Others exhibit abnormal activation of their b-cells—white blood cells which churn out custom-made antibodies to gum up specific pathogens. In these cases, their b-cells seem to make an unusual quantity and variety of “auto-antibodies”, which attack the body’s own cells instead of invaders. Others still have low levels of interferons, a group of molecules involved in fighting off viral infections. And some have problems with their t-cells, which are parts of the immune system that have the jobs of destroying infected cells and alerting b-cells to the presence of pathogens, so that appropriate antibodies can be made.

Several studies have found reduced t-cell counts in people who have had acute covid-19, and also that their surviving t-cells are “exhausted”—meaning they mount only a weak response to infections.
And third:
The third hypothesis about the cause of long covid, inflammation, holds that the fight put up by the body against the acute illness causes irreparable collateral damage. This often happens during a viral infection, but it could be particularly likely with covid-19. Out-of-control inflammation, caused by cytokines (molecules that drum up inflammation) is a hallmark of the illness.

One guess is that the inflammation which happens when people are ill somehow damages parts of their autonomic nervous systems. Another suggestion, made by Dr Koralnik, is that in some patients sars-cov-2 may damage the cells that line blood vessels, either by infecting them directly or via inflammation. This would change the way blood flows to the brain, and may thus explain the brain fog.

The article gave me some hope, especially this part. Hope it's useful for others to read.
Studies intended to investigate each of these possibilities are under way. But the three theories are not mutually exclusive. Indeed, most researchers agree that long covid is probably a term which embraces several conditions with different causes.

Determining these will help both with the development of treatments and with their prescription. If persistent viral infection turns out to be a cause, the search will be on for suitable antiviral drugs. Treatment would consist either of a defined course of medication that clears the virus completely (as is now possible for hepatitis c, for example) or of drugs that people take routinely to keep the virus at bay, the approach taken with hiv/aids...

Treatments for immune disorders already exist, and some may work for long covid. “As soon as we define the immune abnormality in these patients, then it will become very clear how to treat them,” says Dr Nath. “It is quite possible that we may need multiple treatments for different types of immune response—and we should be able to figure that out as well.”
The way I see it, whatever they figure out is ultimately the causative factor for Long-COVID, we could immediately research similarly for ME, aka as it relates to viruses that triggered many of our cases of ME.
 
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Wishful

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Sadly, nothing in that sounds like 'closing in'; they're just some vague hypotheses without solid evidence, which could have been posed as soon as 'long Covid' was accepted as reality. I'm sure there's been some progress in ruling out other hypotheses, and they've been collecting useful data, but I don't get the impression that they're any closer to an answer to the underlying mechanism than ME researchers are.

Long-Covid research teams do have more funding, so that's a positive.
 

sometexan84

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But the three theories are not mutually exclusive.
Glad to see they added this, as I 100% believe it's both that 1st and 2nd theory. The lingering transformed infection, as well as autoimmunity.

Dysfunctional immune system and autoimmunity initiated and perpetuated by the persistent infection.

Enterovirus B is to ME/CFS, as
1626821458949.png

SARS-CoV-2 is to Long Covid

1626821366434.png
I just pray that the covid antiviral (that will for sure come before there's an enterovirus antiviral) will be a more broad spectrum RNA antiviral.
 

Treeman

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I have already tested positive for circulating antibodies and auto anitbodies, I just haven't had more extensive and specific tests and been offered treatments, possibly in part due to them not yet existing. It's good news if it's followed up and all successful. I'll continue to keep my fingers crossed
 

Treeman

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Additionally, there are many reports along these same lines about researchers hypothesising a similar story. However I expect a lot of over lap in their work, so not being collaborative and not using the funds and skills in the most efficient way possible. This worries me.
 

livinglighter

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The UK government is allocating even more money towards long COVID research now they’ve decided to remove COVID restrictions.

They’ve created a COVID vaccine. I believe they will also unravel long COVID. It’s just a shame medics are still referring to it as a brand new syndrome when similar/same hypothesis are proposed for ME.

I don’t want to sound negative but I think ME researchers are going to have the same difficulty with receiving funding for investigating similarities.

Here in the UK they are doing their best to keep both illnesses separate.