The Enterovirus Theory of Disease Etiology in ME/CFS: A Critical Review (O'Neal and Hanson, 2021)

R

Rim1

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Hip said:
Oxymatrine did not help me (my ME/CFS was triggered by CVB4), but then I also have high IgG antibodies to cytomegalovirus, suggesting I have issues with more than one virus.
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That's exactly why I'm interested in a ''universal antiviral'' and I was asking you if tenofovir could also be antiviral against the enteroviruses in the other post.
Also don't get why it's being given so little attention to draco/vtose in the forums (no mention at all in discord).
 
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roller

roller

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Hip said:
but the RNA is not quite fully cleared from the cell, so then the viral RNA regrows back in the same cells once interferon therapy is over.
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Pyrithione may contribute to clearance

it doesnt show this info on wiki.
it was a study. and the non-clearance had also some unbeneficial effect on nalphakappa(.?...)pathway.
 
Hip

Hip

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Pep1 said:
That's exactly why I'm interested in a ''universal antiviral'' and I was asking you if tenofovir could also be antiviral against the enteroviruses in the other post.
Also don't get why it's being given so little attention to draco/vtose in the forums (no mention at all in discord).
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I have not seen any studies showing tenofovir is antiviral for enterovirus, but tenofovir might fight enterovirus by boosting the immune response. Some drugs are directly antiviral (inhibit the viral lifecycle), and others are immunomodulators which can fight infections by ramping up the immune response.

DRACO did receive some attention on this forum when its inventor Dr Todd Rider proposed it, there are some old threads on DRACO; but his research seems to have come to a halt. The idea was recently taken up by a new team in New Zealand, in the form of Vtose (see this thread). Some have considered a custom synthesis, but I would not want to be the first person to try a drug which contains a molecule that triggers apoptosis.



roller said:
Pyrithione may contribute to clearance
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I think you may mean this paper, which found that zinc ionophores pyrithione and hinokitiol inhibit picornavirus (the family to which enterovirus belongs).

Zinc ionophores import zinc into cells. Unfortunately zinc pyrithione (a chemical found in anti-dandruff shampoos) was found to deform the spines of rats when taken internally.

There are other zinc ionophores like EGCG and hydroxychloroquine, but I noticed no benefits from high dose EGCG (except that it has an antidepressant effect).
 
Nuno

Nuno

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Pyrrhus said:
Unfortunately, molnupiravir is a mutagenic nucleoside analogue, so there is a large risk that it will not pass safety trials. But let's certainly hope for the best!
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Hey Pyrrhus, a few months have passed since you posted about Molnupiravir, and turns out it's actually doing pretty well on trials so far.

Has your position changed towards this possible treatment? Interested to hear!

Regards,
Nuno
 
Pyrrhus

Pyrrhus

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Nuno said:
Hey Pyrrhus, a few months have passed since you posted about Molnupiravir, and turns out it's actually doing pretty well on trials so far.
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Here are the published results from the Phase I trial, which reported that low doses of the drug were well tolerated:
https://journals.asm.org/doi/full/10.1128/AAC.02428-20

The question in my mind is whether the doses and dosing frequency in the trial were high enough to be effective against the coronavirus. I don't know if molnupiravir has yet been tested against any enteroviruses.
 
RYO

RYO

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Recent MECFS webinars that featured Dr Nath and Dr Hansen reported that there is reproducible mitochondrial defect in immune cells of MECFS patients. Dr Hansen’s paper on enterovirus alludes to the fact that latent enterovirus infection may alter mitochondrial function. I doubt the NIH will pursue the hypothesis that some MECFS patients may have chronic enterovirus infection. However, hopefully Dr Hansen will get enough funding to further explore this possibility.
 
Pyrrhus

Pyrrhus

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RYO said:
Dr Hansen’s paper on enterovirus alludes to the fact that latent enterovirus infection may alter mitochondrial function.
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One important caveat to keep in mind:

Enterovirus infection of a cell only impairs mitochondrial function in that cell.
It wouldn't cause widespread mitochondrial dysfunction throughout the body.

...that is, except perhaps if it leads to long-lasting inflammation that, over a long period of time, eventually depletes key metabolites needed by mitochondria in the rest of the body...
 
RYO

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That is another key question that needs to be answered. Is there something in the plasma or serum that is deleteriously affecting mitochondrial function or something intracellularly? Is there a signal that promotes inefficient mitochondrial function (mitochondrial fission)?
 
B

bread.

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Pyrrhus said:
One important caveat to keep in mind:

Enterovirus infection of a cell only impairs mitochondrial function in that cell.
It wouldn't cause widespread mitochondrial dysfunction throughout the body.

...that is, except perhaps if it leads to long-lasting inflammation that, over a long period of time, eventually depletes key metabolites needed by mitochondria in the rest of the body...
Click to expand...

What is your take, if you have one, on the mitochondrial dysfunction present in me/cfs cd8 cells for example?

Seems unlikely to be due to "inflammation"?
 
EddieB

EddieB

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There is a thought, or theory, that by-products of the infection(s) produce things like D-lactic acid, and other organic acids and compounds, that cause a “sick syndrome” feeling throughout the body. Essentially telling everything to shut down and go into a conservation mode of self protection. And that this could become a chronic or even overreactive state.
Judging from my own symptoms, this sounds like what’s happening, but I have no idea if it’s actually true.
 
Pyrrhus

Pyrrhus

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bread. said:
What is your take, if you have one, on the mitochondrial dysfunction present in me/cfs cd8 cells for example?
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I am trying to keep an open mind, as there are a lot of unanswered questions here.

The biggest unanswered question is whether the findings of mitochondrial dysfunction are really unique to ME or whether they are also seen in many other chronic conditions.

bread. said:
Seems unlikely to be due to "inflammation"?
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It seems unlikely to be due to short-term inflammation, but long-term oxidative stress, such as from chronic inflammation, is another matter.

Long-term oxidative stress in any part of the body, such as from chronic inflammation, is known to deplete metabolites throughout the body. These metabolites might be needed for mitochondrial function. So it is indeed possible that the observed mitochondrial dysfunction present in ME blood cells is a downstream effect of long-term oxidative stress or chronic inflammation in a part of the body.

As always, more research is needed...
 
RYO

RYO

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As I rewatched the webinar “Advances in our understanding of MECFS and the effects long COVID”, I found Maureen Hanson’s presentation about changes in the microbiome very interesting. She mentions that other disease states such as inflammatory bowel disease, HIV infection, non alcoholic fatty liver disease and Parkinson’s disease can lead to similar microbiome dysbiosis. What if the potential trigger for most of these diseases is a chronic latent infection of the gastrointestinal tract. Perhaps the viral trigger is not always a species of enterovirus but the end result is the same.

I think the importance of interactions/cross talk between the gut, brain, and immune system will make themselves evident as researchers continue their efforts to understand complex biologic systems. A first step might be to obtain tissue samples from the stomach and colon of MECFS patients. However, I suspect someone may need to develop a new technology to study complex interactions between the gut microbiome, immune system and the brain.
 
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halcyon

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Pep1 said:
Has Chia also made the tests in normal people to see if they also have chronic enteroviruses? Maybe most of the population has them.
And then maybe all of CFS people have more than one enterovirus causing it(not calculating those who have herpesviruses causing it for example).
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Yes, he has, and no, they don't.
Chia_J._EV_serology.png


One of the more interesting studies (Galbraith et al., 1995) from the 90s that was completely ignored is the one showing that the enteroviruses isolated from ME patients are largely genetically distinct from known wild-type acute infections.
galbraith1995.png
 
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