Possible chronic viral infection in ME/CFS (& other illnesses inc Long covid). Discussion.

Michiel Tack said:
If all of the illnesses caused by chronic viral infections don't look like ME/CFS or share some of its core features, then I would think this is quite relevant to the discussion.
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this comes back to the point that I was trying to make here. You are assuming that the chronic infections we know about amount to ALL chronic infections so ME/CFS has to look like them (though I don't think that's true: even for acute infections, viruses can present in many ways). Nath is exploring the possibility that Long Covid involves chronic infection undetectable by current methods. If that's right, as I said, it would be a new paradigm.

Clearly, Nath thinks this idea is worth exploring, and he's a leading virologist with a vast amount clinical experience. I'm sure he's well aware of the current range of chronic viral infections and yet he is considering an undetected chronic viral infection as a possibliity to explain long Covid, which happens to look a lot like ME/CFS. Perhaps the most important thing here is that he is going to be testing the hypothesis. I guess we should know within a couple of years or so if it's right or not.

Added: it's precisely because someone like Nath is taking the chronic infection hypothesis seriously that I started this thread.

Michiel Tack said:
I thought that in the cases of a well-adapted chronic infection the illness is significantly less severe than ME/CFS. And in cases where it gets as severe as ME/CFS it is usually a process that causes visible damage or makes patients progressively worse over time.
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that's a fair point. But you were arguing a chronic virus had to be progressive. There are plenty of asymptomatic chronic viral infections, including adenoviruses. Adaption is a matter of time. We had a adenoviruses since before we split from chimpanzees a couple of million years ago (The Oxford vaccine is based on a chimp adenovirus). So it's logically possible for a chronic infection to have started the adaption process to the point it isn't a progressive disease, killing its host, but without being asymptomatic and still being quite severe.

Andy said:
So perhaps Math should be looking for other, opportunistic, pathogens other than just viruses.
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I can't be certain, but I think the kind of broad approaches that Nath is using would pick up other pathogens as well.
 
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I think Michiel has the right analysis here. If even a significant subset of ME/CFS was due to persistent viral infection somewhere sometime someone would have found some barn door pathology in a case that got so bad the pathology showed up.

All the chronic viral illnesses end up with barn door pathology in at least a proportion of cases.
EBV is a chronic infection that lasts a lifetime but it does not cause any problems as such and there is no pathology.

For me the other weight against the chronic viral idea is that for the last sixty years (my mother being an EBV virologist) I have been aware of people trying to explain the unexplainable with chronic viruses for no better reason than viruses are small and can hide. Exhaustive studies of these conditions came out blank.

For me as a birdwatcher it is a bit like asking if the bird on the peanut feeder is likely to be a stork. If it is small and green-yellow the chances aren't very high!!
 
@Simon M Should your list include Williams & Ariza @ Ohio - they have done some very interesting work on EBV. They, along with Prusty for HHV6 (snc-U14), have been looking at the effect of viral proteins on cells / body / mouse model.

E.g.
Epstein-Barr Virus dUTPase Induces Neuroinflammatory Mediators: Implications for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
https://www.clinicaltherapeutics.com/article/S0149-2918(19)30173-0/fulltext

ETA : List of Williams/Ariza publications on NIH reporter for their NIH grant funded project
https://reporter.nih.gov/search/naiwnO2GzU2dDE8wFFPDyA/project-details/10049715#publications
 
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Jonathan Edwards said:
f even a significant subset of ME/CFS was due to persistent viral infection somewhere sometime someone would have found some barn door pathology in a case that got so bad the pathology showed up.
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That would make sense if this was an illness where really bad cases were properly investigated – instead of being told they were too ill to be seen.

It was interesting that in the case of the persistent dengue fever Nath quoted, even the specialist clinical team at Bethesda couldn't find it while the patient was alive and only found it through an autopsy.

I should say I'm not at all convinced by the chronic viral theory, but at the same time, I don't think we should completely dismiss it either. In any case, we should be getting an answer for Long Covid before too long. Let's see.
 
Simon M said:
That would make sense if this was an illness where really bad cases were properly investigated – instead of being told they were too ill to be seen.
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Of all of the millions of PWME over the last five decades a few would have shown up virus used pathology if it was there. We have a few post mortem cases diagnosed in life as ME, with some odd neuropathological changes but nothing that really looked viral or really explained the illness.

It seems to me that if one is going to pursue a theory about a causal class like viruses one needs to have at least some indicative data.Otherwise why not go for prions or something not yet recognised?

Simon M said:
It was interesting that in the case of the persistent dengue fever Nath quoted, even the specialist clinical team at Bethesda couldn't find it while the patient was alive and only found it through an autopsy.
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So in this case presumably there was barn door pathology? Or if not how do we know the virus was relevant? One off stories like that merit a good degree of scepticism in boy book.

We shouldn't dismiss anything but if you are putting bets on a horse race you tend not to put your money on a 32 year old nag with laminitis!
 
Jonathan Edwards said:
Of all of the millions of PWME over the last five decades a few would have shown up virus used pathology if it was there.
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Some PWME have persistent virus identified by PCR such as EBV and HHV6. Some respond to antivirals and some don't.

Jamison wrote just yesterday that he may have passed on some of his viral pathology to his girlfriend the one time she came to visit and ME clinicians seem to have confirmed that this could be the case as he has had active virus in blood test results.
What we didn’t realize was that I could have given her a virus other than Epstein-Barr. Since I last saw her, I’ve tested positive for other viruses, including cytomegalovirus and parvovirus, both of which, like Epstein-Barr, become latent by the time most people enter adulthood. But for some reason, they too still show up acutely in my blood work.
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wigglethemouse said:
Some PWME have persistent virus identified by PCR such as EBV and HHV6. Some respond to antivirals and some don't.
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As I said, some viruses like EBV persist and that is normal. If they are associated with illness they are associated with measurable pathology (not just antibody titres, pathology). So if ME shows no pathology of the sort we see with viral damage to cells then it doesn't fit.
 
Simon M said:
this comes back to the point that I was trying to make here. You are assuming that the chronic infections we know about amount to ALL chronic infections so ME/CFS has to look like them (though I don't think that's true: even for acute infections, viruses can present in many ways). Nath is exploring the possibility that Long Covid involves chronic infection undetectable by current methods. If that's right, as I said, it would be a new paradigm.

Clearly, Nath thinks this idea is worth exploring, and he's a leading virologist with a vast amount clinical experience. I'm sure he's well aware of the current range of chronic viral infections and yet he is considering an undetected chronic viral infection as a possibliity to explain long Covid, which happens to look a lot like ME/CFS. Perhaps the most important thing here is that he is going to be testing the hypothesis. I guess we should know within a couple of years or so if it's right or not.

Added: it's precisely because someone like Nath is taking the chronic infection hypothesis seriously that I started this thread.

that's a fair point. But you were arguing a chronic virus had to be progressive. There are plenty of asymptomatic chronic viral infections, including adenoviruses. Adaption is a matter of time. We had a adenoviruses since before we split from chimpanzees a couple of million years ago (The Oxford vaccine is based on a chimp adenovirus). So it's logically possible for a chronic infection to have started the adaption process to the point it isn't a progressive disease, killing its host, but without being asymptomatic and still being quite severe.

I can't be certain, but I think the kind of broad approaches that Nath is using would pick up other pathogens as well.
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Is this not linked to Prusty's hypothesis that you have latent infection and this causes the downstream effect i.e. ME/CFS? I assume Prusty's controversial (Robert Phair didn't agree) invitation to speak at the NIH symposium - 2 years ago(?)- was due to Nath's interest.

Will GWAS help to resolve the question of whether virus's are significant or a study of HLA/KIR sequences [think OMF/Mark Davis is looking at KIR]?
 
Jaybee00 said:
The positive response to anti-virals is likely due to a mechanism *not* related to killing/ inhibiting viruses. This was pointed out by Naviaux, but I can no longer find it on his website.
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I don't think we actually have evidence of response to anti-virals. Moreover, I cannot make sense of Naviaux's comment there - he says that responses must indicate persistent virus but then suggests that the drugs are working through other routes - so where is the evidence for persistent virus?
 
These researchers seem to be very specifically drawn as those who are interested in viruses, so it's not surprising that they would float the idea of viral persistance.

Nath is basically only interested in studying post-viral me/cfs, hence the intramural entry criteria.

Dr. Avi Nath: Dealing with a lot of different diseases, that's not my area of expertise. I'm not a lymphoma expert. My area of expertise is infections and so that's why we've established a cohort of ME/CFS patients who clearly had an infectious process and then developed that and the COVID patients again very clearly, they had an infectious process and now they're developing symptoms that look like ME/CFS. So for me that makes the most sense to use my expertise to study those kinds of patients. Lymphoma patients other people should study if they have that kind of expertise.
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MVE has never produced any research on this 8-year old hypothesis and Prusty suffers the same focus as nath except on a specific virus and it's interactions with mitochondria.
 
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wigglethemouse said:
Some PWME have persistent virus identified by PCR such as EBV and HHV6. Some respond to antivirals and some don't.

Jamison wrote just yesterday that he may have passed on some of his viral pathology to his girlfriend the one time she came to visit and ME clinicians seem to have confirmed that this could be the case as he has had active virus in blood test results.

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Did she have me/cfs before, though?
 
Sorry for sending the thread of track. What I was trying to get across was that a small number of ME patients have positive PCR showing active virus in the blood and in those antivirals (including the IV type) don't always result in a negative PCR test. I was not talikng about IgG or IgM etc results on which some clinicians in the past based antiviral treatments on.
 
Andy said:
I understand that I'm heading off-topic somewhat here but I think there is value in highlighting something that Karl Morton is interested in, which is L-form bacteria. If I'm remembering correctly, these are cell wall-less pathogens which are hard, or impossible, to detect using standard techniques. A company in the States was looking into the existence of these alongside chronic illnesses, such as FM and ME, and the, admittedly limited, results they have so far suggest that those with chronic illnesses also have higher numbers of L-form bacteria in their system.

Obviously, like any new area of research, there is, for me, a reasonable question as to whether they have discovered something new, or if it's an artefact of the ways of testing that they use, or some other reason for not being the case.

But one hypothesis is that these L-form bacteria might be able to take advantage of a disruption of the immune system, such as a viral attack, which normally keeps them in check, and that they then multiply, causing increased issues.

And obviously if the focus, from the immune system and doctors, is on the viral attack, then no attention is paid to other pathogens. So perhaps Math should be looking for other, opportunistic, pathogens other than just viruses.

I'll try to return and add links to what research is out there on this later, can't do that at the moment.
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from memory ( so may be wrong as it's currently 4.15am and little sleep ) from plant research L form bacteria have a weird way of combining with proteins and this can be used to develop disease resistance

Sleep deprived thought- if there is a weird protein mechanism does this circle back to misfolded proteins possibilities....

Eta spelling
 
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Andy said:
I understand that I'm heading off-topic somewhat here but I think there is value in highlighting something that Karl Morton is interested in, which is L-form bacteria. If I'm remembering correctly, these are cell wall-less pathogens which are hard, or impossible, to detect using standard techniques. A company in the States was looking into the existence of these alongside chronic illnesses, such as FM and ME, and the, admittedly limited, results they have so far suggest that those with chronic illnesses also have higher numbers of L-form bacteria in their system.

Obviously, like any new area of research, there is, for me, a reasonable question as to whether they have discovered something new, or if it's an artefact of the ways of testing that they use, or some other reason for not being the case.

But one hypothesis is that these L-form bacteria might be able to take advantage of a disruption of the immune system, such as a viral attack, which normally keeps them in check, and that they then multiply, causing increased issues.

And obviously if the focus, from the immune system and doctors, is on the viral attack, then no attention is paid to other pathogens. So perhaps Math should be looking for other, opportunistic, pathogens other than just viruses.

I'll try to return and add links to what research is out there on this later, can't do that at the moment.
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Info on L form.bacteria
https://royalsocietypublishing.org/doi/10.1098/rstb.2015.0494

Marshall Protocol also has info
 
https://www.s4me.info/threads/rever...tient-derived-tissues-2021-zhang-et-al.20768/
"Reverse-transcribed SARS-CoV-2 RNA can integrate into the genome of cultured human cells."

This popped up elsewhere and I thought it was worth linking here as it suggests a mechanism whereby viruses might persist without being detectable in the blood.


I am a barn door recurring virus case. Yet I feel like everyone seems to ignore me, I am selectively Bowdlerised from medical awareness possibly because of prudishness since I have a provenly recurring STD
and feel like Oscar escaping from Reading jail everytime I mention it
m3pt6LN.jpg
love you Banksy

on top of which I feel like I have recurring EBV and previously had recurring swineflu for seven years and post covid I have something else recurring which I expect is covid. I cant prove the rest of them but I can prove the HSV2 and even that was flatly disbelieved for 20 years despite the proof, only for people to turn around and say "oh yes that can happen" decades later.

The viruses compete to trigger my immune defences so if I have one recurring quicker than the others then it blots out the others, trouble is this is a ratchet effect and I appear to be down to about 6 days cycle now with covid. If that alleviates then a different virus recurs like my HSV2 which has a 30-45 day cycle. The recurring swineflu was interestingly temperature dependant though seems to have attenuated now at last which took a while but previously I had to raise the temperature of my environment to 27°C to be sure I did not come down with a full blown head cold every few weeks (honestly prefer the HSV2) and lived my life wrapped up in acrylic fleece.

If people choose to ignore evidence of recurring viruses then they are not going to see any. That is like looking at a three foot high bird with white and black plumage and a long yellow beak standing on your bird table and saying its probably a big finch. Which is to say if one takes the opinion of revered authorities as a guide in interpreting observations then one runs the risk of becoming trapped by past dogma.

I am absolutely certain that I have recurring viruses and have met others with the same condition and I wonder how many people are out there who dare not speak of this condition where it relates to an STD, its not the sort of thing people want to be known for but looking at it from the detached perspective I was encouraged to adopt as an undergraduate reading zoology its supremely logical for HSV2 to behave this way, its what it has evolved to do, take advantage of the human sex drive to replicate itself, reactivating at (in)opportune moments.

I am sure there is a subtype of ME aka CFIDS which has a problem with recurring virus, not necessarily related to the STD HSV2 but related to recurring virus nonetheless but what I dont know is how many other people have the same problem and what proportion we are of all ME cases.

There is much more to say about other kinds of condition which could also trigger the immune system to produce ME symptoms but there is only so much one can broach in a post and maintain a discussion, which I would like to do. Suffice to say I think at least some ME cases are due to recurring viruses but maybe not all.
 
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Michiel Tack said:
I had the impression that those who get progressively worse form a subgroup and not the majority but it is difficult to say because we have little good data on prognosis.
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We have basically zero reliable data on ME disease progression. There's also an important distinction, I think, between those who are able to pace and manage their disease, and those who cannot but push through due to socioeconomic circumstances and/or institutional pressure and thereby drive themselves deeper into the ME hole. Overexertion followed by a failure to recover to baseline equals worsening. That's certainly how it's been for me, 11 years and counting. But even setting aside the effect of continual PEM, I think it's difficult to say whether textbook ME is progressive or static.

Lastly, I think we as a patient / research community should be mindful of survivorship bias. I'm sure you're all familiar with the famous WWII example of bullet holes on damaged aeroplanes. Patients who died either directly or indirectly from ME because their disease progressed... The dead don't talk. In fact, the severely ill don't talk either. And God only knows how many are in that condition, what their original baseline was, and where they are headed.
 
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