Do you believe that “viral persistence” is the cause of ongoing MECFS and LC?

From a conversation between John Chia and Amy Proal a couple years ago, he discusses finding it in the gut, and that even knowing where to look, it's hard to detect:

 

So then do you think the reason for fatigue in sickness behavior is not the body's attempt at energy conservation/redirecting energy? That it's mostly something else like the virus directly causing fatigue, or the body making one tired to prevent infecting others? Or you just haven't seen good evidence either way?

 

Nobody has any way of knowing I suspect. But considering the evolutionary pressures that might make a sickness response useful my guess would be that if you have active infection it is a good idea to curl up in a cave and wait for the immune system to do its work rather than trying to hunt for some more food simply because you would be exposing yourself to dangers while functioning poorly. As much as anything it might be a way of making sure you and your family do not eat any more of that rotten meat.

A major part of the sickness response is stopping eating, so it is hard to argue that it is there to make sure energy is available. Energy intake is shut down.

 

There are most likely some pwME who are infected with enterovirus. I would imagine that they would need many tissue samples in various areas of the gut to detect it.

Have you seen the discussions on this thread

 

I assumed digestion costs significantly more available energy per ATP produced than using fat reserves, so the body might switch to the cheaper ATP for a short time. I'm not finding research about relative energy costs, though...

 

Interesting, although in that quote he cites his study that didn't find viruses. But as the researchers above are saying, it's likely if there are viruses, it'll require deeper searchers and improved techniques to find them.

 

I suspect that there are, at least in some pwME, multiple pathogens (viral, bacterial and/or parasites) simultaneously at play. It may be a crap shoot trying to figure which one, or which combination, cause symptom persistence since diagnostics can be wholly inadequate.

 

https://twitter.com/user/status/1846675566184771746


Dr. Maayan Levy joins the Arc Institute as an Innovation Investigator, with a Stanford Pathology appointment expected in January 2025. Her work on viral persistence and serotonin reduction in #LongCovid remains highly impactful.

probably goes under the Arc thread.

 

Lots of people with ME/CFS get sore throats, right? I do. Sometimes immediately after hours of continuous computer use. And sometimes upon waking up after too much physical activity the previous day.

Is this potentially a good location to look for viruses?

StatPearls: Pharyngitis, 2023, Wolford et al

So given a sore throat in someone in the general population, the most likely cause is a virus. Maybe doesn't translate to ME/CFS. But maybe it does.

And if a virus is the cause, there's a good chance the virus is in the throat itself.

Maybe a sore throat is a rare time that a persistent virus comes to an easily accessible location, and can be detected with a throat swab. (Or maybe biopsy, but that sounds very invasive and unpleasant.)

If a study finds that throat cultures of people with ME/CFS show higher viral levels after exercise, this might be useful for PEM and viral persistence research.

 

I'm kind of surprised no one responded to this. I thought it was a pretty good idea. Are there reasons this wouldn't be worth doing?

 

That does sound like an interesting proposal.

Sorry I tend to sometimes skim these more speculative threads but rarely read them more thoroughly as to be honest I have little clue what I’m talking about.

In my opinion, I think it’s more likely the sore throat arises from some kind of weird immune response, similar to how people with Sjörgen’s Syndrome and Lupus can have sort throats, or perhaps it could be some novel mechanism we have no idea about.

But throat culture studies sounds like a cheapish way to look into persistence and PEM, so I would be interested in it.

 

Thanks for the reply and pointing out those conditions. Interestingly, I found a reddit thread about sore throats in lupus and the top two comments are saying they get a sore throat following exertion.

 

The second comment especially sounds exactly like a manifestation of PEM!

 

It's been about a year since I last posted this. Much more research has some out, but I still believe the same. They've found precious little evidence for it. It's very unlikely that ongoing infections or viral persistence drive ME or LC. The one trial of Paxlovid in LC that completed failed (S4ME thread)

 

I just finished listening to the latest PolyBio symposium, and I came away from it with almost the opposite feeling. Talk after talk mentioned finding various components of SARS-CoV-2 in various tissues long after the infection. As well as some talks about irregularities with other viruses, like EBV.

I definitely couldn't fully focus on it due to brain fog, so I may be misintepreting/misremembering the extent of researchers findings of viruses.

 

That was my impression too @forestglip. Here are the talks relating to viral persistence (the majority).

If you were only going to watch two, I would probably highlight the first talk by Morgane Bomsel on her work with Dominique Salmon in Paris on SCV2 persistence in megakaryocytes and John Wherry's T cell biosensors.

50:47 Morgane Bomsel–MEGALONG Study: SARS-CoV-2 Persistence & Impact on Long COVID Megakaryocytes & Platelets
1:02:57 Johan Van Weyenburg–Blood transcriptomics reveal persistent SARS-CoV-2 RNA as a candidate biomarker, a real world Long COVID cohort

1:17:35 Marcus Buggert–LymphPASC Project Proposal: Exploring Lymphoid Immune Activation in Post Acute COVID-19
1:41:42 Akiko Iwasaki–Probing the Role of Endogenous and Latent Viruses in Long COVID
1:52:30 John Wherry–T cells as biosensors in Long COVID
2:04:32 Michael Peluso–LIINC Updates, Expansion of LIINC to ME/CFS, Targeting the SCV2 Resevoir in Long COVID Clinical Trial
2:17:18 Tim Henrich–Molecular Imaging in Long COVID & Tissue Biopsy Program Updates

2:29:19 Esen Sefik–Dissecting Disease Mechanisms of Long COVID: Myeloid resevoirs of SCV2
3:03:17 Lael Yonker–Updates for Pediatric Long COVID

3:46:05 Zian Tseng–POstemortem Systematic invesTigation of Sudden Cardiac Death Study (POST SCD)
4:11:52 Chiara Giannarelli–Cardiovascular complications of COVID 19
4:24:39 Chris Dupont–Tissue Profiling Pipeline for Infection-Associated Chronic Conditions

5:08:19 Nadia Roan–SARS-CoV-2 persistence and T cell activity in the female reproductive tract
5:20:23 Alessio Fasano–Larazotide Improves Spike Clearance & Augments Recovery from Post Acute Sequalae of COVID
5:31:09 Sara Cherry–Long COVID: Defining a Viral Resevoir in the GI tract

 

Long COVID appears to be driven by ‘long infection’. Is that what the science says?


https://marcveldhoen.substack.com/p/long-covid-appears-to-be-driven-by

 

"Infection-associated" does not mean that an infection is still be present, although the finding of T cell exhaustion in our work and that of others is consistent with this possibility. Additional research comparing ME/CFS to other IACCs is essential!
https://twitter.com/user/status/1863713763028799510

 

Do we really need to disprove? We typically assume X is false and then try to prove otherwise. There have been more than adequate attempts at proving viral theory in the past 40 years, that I think it's past time to lay it to the rest. I'd rather see the money go into something newer and more promising.

 

There have been almost as many papers on long COVID (6,564) in 4 years as there were on CFS in the 33 years from 1987 to 2020 (7101). And as far as I know, it still took until 2024 to report that SARS-CoV-2 antisense RNA can persist long after infection in humans. And in the case of COVID they have the advantage of knowing exactly which virus to look for, and have access to better technology than was available to ME/CFS researchers in the past.

Not to say it's known that viral persistence causes long COVID, just illustrating that it can be very hard to find a virus in the body.