Preprint Virus Genome Sequences in the Blood of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients, 2025, Davis et al

hotblack said:
It looks like they were all severely ill and visited in their homes which may impact viruses exposed to? But I guess cause/effect/chance is difficult to be sure of.
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Do less viruses in the blood of ME/CFS patients mean something about their immune system or is the most likely explanation less contact with other people and therefore less exposure to viruses?
 
Of course it may well be what @ME/CFS Science Blog suggests : Fewer contacts of patients means that the probability of infection is very low. However, I would like to mention a subset of ME/CFS patients who say that ever since they gotten ME/CFS they do not get viral infections at all. I wonder whether this is a clue and this subset may be deserving more attention.

It is possible (?) that we are looking at impaired N-Linked glycosylation which is a key mechanism used by enveloped viruses to attach to a host. I believe there is only one study at the moment which is looking at glycosylation function in ME/CFS patients
 
BrightCandle said:
But I suspect everyone is just walking around with a collection of low level infections of all sorts
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Our gut is full of all sorts of phages, so wouldn't the rest of our body be too? Our gut immune cells apparently grab bacteria (and maybe other microbes?) and drag them to our (was it thymus?) glands to teach new cells to ignore them. "Hey class: meet G45d565treew55yu. He's a good guy!" So, are the beneficial microbes populating us considered "infections"? I really like those bacteria (mitochondria) infecting my cells.

Do beneficial viruses exist in our cells? That would complicate studies of this type, especially if specific viruses were beneficial in specific individuals, and detrimental in others.
 
Creekside said:
https://sciencedaily.com/releases/2025/11/251102205009.htm

"The researchers studied bacteria that carry extremely old, inactive viruses and found that these dormant invaders still play a protective role." Maybe our cells have these too. Isn't a lot of our DNA old viral fragments? More DNA/RNA to mess up studies if they're not accounted for properly.
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Google says 8 % is from viruses, and another 40 % is just repeating letters thought to also be from viruses. No idea if that could lead to false positives in those experiments.
 
DMissa said:
What we can can say is that attempts to demonstrate the presence of the thing continue to fail.
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In blood, @DMissa , in blood. Some things gravitate away from blood; you won't find them there.

Who was it 15 or so years ago that admonished the then CFS research community to not look at tissue?

Look at tissue. Comprehensively.

Then we can talk.
 
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duncan said:
In blood, @DMissa , in blood. Some things gravitate away from blood; you won't find them there.
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Even viruses that establish chronic infection in the tissues release viral RNA into the blood. Hep C for example is diagnosed with blood antibody and RNA tests. Pretty much the only place you could reasonably expect to have active viral replication with little detectable RNA in the blood is if it was in the brain.

The most likely examples we have of viruses actively replicating long term in the brain—such as HIV and Zika—both present with very different clinical pictures from ME/CFS in terms of their associated neurological impacts. Progressive worsening, dementia-like memory loss, severe developmental issues in fetal cases, etc. Since people get ME/CFS from many different viruses, each with very different properties such as what type of cells they can infect, it becomes even more of a pipe dream to explain how they all somehow set up shop in the brain for years and all end up leading to a phenotype like ME/CFS.

Looking in specific tissue based on a strong hypothesis could well be fruitful. Looking in every tissue, invasively, for a viral theory that doesn’t really add up even on paper…I’m not sure there’s any convincing argument to be made for putting more of a limited supply of eggs in that same basket after this study.
 
jnmaciuch said:
Even viruses that establish chronic infection in the tissues release viral RNA into the blood. Hep C for example is diagnosed with blood antibody and RNA tests. Pretty much the only place you could reasonably expect to have active viral replication with little detectable RNA in the blood is if it was in the brain.

The most likely examples we have of viruses actively replicating long term in the brain—such as HIV and Zika—both present with very different clinical pictures from ME/CFS in terms of their associated neurological impacts. Progressive worsening, dementia-like memory loss, severe developmental issues in fetal cases, etc. Since people get ME/CFS from many different viruses, each with very different properties such as what type of cells they can infect, it becomes even more of a pipe dream to explain how they all somehow set up shop in the brain for years and all end up leading to a phenotype like ME/CFS.

Looking in specific tissue based on a strong hypothesis could well be fruitful. Looking in every tissue, invasively, for a viral theory that doesn’t really add up even on paper…I’m not sure there’s any convincing argument to be made for putting more of a limited supply of eggs in that same basket after this study.
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From what I've seen the people in favour of those theories tend to not argue for HIV or Zika as examples, but rather for things like Ebola, which seems to be able to establish itself in certain immunprivileged sites without leaking out into the blood and without causing progressive worsening (but of course it does raise the question whether it causes any symptoms at all and are these in any way a meaningful comparison to ME/CFS symptoms) or they talk about some unfalsifiable hypothetical role of Herpesviruses.

I think the ideas tend to be something like: There is a virus hiding in a specific regions and it then causes body wide symptoms rather than region specific symptoms because there is some subtle change in immunological things that travel. But it never seems to answer the question: It seems a whole host of infections (and maybe some toxin exposures or similar) are able to cause these symptoms so it can't really be virus specific, so why not just look for the immunological changes if the viruses are anyways never found?

I'm not in favour of said ideas, but I do think their examples they use tend to be different, even if typically not meaningful as they tend to be unfalsifiable. I think even if you'd have looked at specific tissue the argument would then be, the methods weren't sensitive enough.
 
jnmaciuch said:
Even viruses that establish chronic infection in the tissues release viral RNA into the blood. Hep C for example is diagnosed with blood antibody and RNA tests. Pretty much the only place you could reasonably expect to have active viral replication with little detectable RNA in the blood is if it was in the brain.
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What if there is very little - next to none - replication going on? Just bleb aggregates that accrue over time in biofilms in the brain? Viral RNA released into the blood does seem like a compelling rebut, but in the absence of replication?.

I am fascinated by a theory of immune tolerance. Not so much the one that recently won the Nobel Prize; a version that predates that by around three quarters of a century. Basically it suggests that due to properties inherent to the virus/bacteria/parasite, the body's immune reaction to that agent is suppressed.

It proposes that infectious neuro-tropic agent gets into our brain, often without much immunolgical noise. And it stays there; it is not cleared. None of the typical immunological responses occur, there is no abnormal bloodwork, no antibodies, no inflammation. But a slow chronic incapacitation overtakes the infected. Without the benefit of immune fingerprints.

This was talked about back in the 50's, during the height of the Cold War, but it doesn't appear to have gotten much traction in the public, perhaps for good reason. I'm still researching it, but it's a slow go with my brain. I don't know how issues such as the release of viral RNA into blood impact the theory. There is not a lot written on it that I can find.

But, it's fascinating because I can see it potentially fitting - even with the timing of the Royal Hospital outbreak back in the '50's. And it presupposes a persistent infectious agent.

Is it right? Probably not. But it's possible. Ultimately it's merely one more theory in a long string that I've been trying to get my arms around , with an eye to confirming or debunking.
 
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EndME said:
From what I've seen the people in favour of those theories tend to not argue for HIV or Zika as examples, but rather for things like Ebola, which seems to be able to establish itself in certain immunprivileged sites without leaking out into the blood and without causing progressive worsening (but of course it does raise the question whether it causes any symptoms at all and are these in any way a meaningful comparison to ME/CFS symptoms) or they talk about some unfalsifiable hypothetical role of Herpesviruses.

I think the ideas tend to be something like: There is a virus hiding in a specific regions and it then causes body wide symptoms rather than region specific symptoms because there is some subtle change in immunological things that travel. But it never seems to answer the question: It seems a whole host of infections (and maybe some toxin exposures or similar) are able to cause these symptoms so it can't really be virus specific, so why not just look for the immunological changes if the viruses are anyways never found?

I'm not in favour of said ideas, but I do think their examples they use tend to be different, even if typically not meaningful as they tend to be unfalsifiable. I think even if you'd have looked at specific tissue the argument would then be, the methods weren't sensitive enough.
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yeah, I didn’t see those arguments as particularly convincing either—Ebola is a unique case because its target cell type is myeloids, which are integrated into the barriers of these immunoprivileged sites. And a quick google confirms that the chronic symptoms of Ebola [edit: if and when they occur] tend to be specific to these privileged sites—eye and joint problems, etc.
 
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duncan said:
What if there is very little - next to none - replication going on? Just bleb aggregates that accrue over time in biofilms in the brain?
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Fragments of inert viruses do hang around for a long time after the infection has cleared. But the scenario in which they cause long term health problems is if they are recognized as pathogenic and induce an immune response. If the fragments themselves are not inducing an immune response, they’re no different to the regular junk proteins that all of our cells already churn out on their own and can handle just fine.
 
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