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

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

  • Yes

    Votes: 16 21.3%

  • No

    Votes: 59 78.7%
  • Total voters
    75
Obviously viruses play a significant role in the genesis of ME/CFS, but I am not sure that a dormant virus lurking unseen in the brain or in some other organ is sufficient to explain all the symptoms of ongoing ME/CFS.

If there was significant viral activity all the time that would surely have been picked up by now, and though we perhaps need more investigation I suspect viral reactivation during PEM or during an ME relapse in those that experience relapses would also have been found.

However there are plenty of other questions:
  • has everyone with ME always been subjected to prior EBV exposure even if that was not the immediate trigger for the condition as may be the case with MS? This might be easier to answer with the larger numbers of Long Covid suffers including many people with an ME like illness not immediately triggered by EBV.
  • can any virus trigger ME onset or an ME relapse, even without prior EBV exposure? My initial onset was associated with Glandular Fever (active EBV infection) but a very significant relapse was associated with influenza.
  • are there ways of identifying very low levels of virus activity that is very localised in the body? The only way I could envisage low levels of viral activity causing ongoing ME symptoms, would be if it was very localised, say in part of the brain that could be demonstrated to be upstream to all the varied symptoms experienced
  • etc
 
Peter Trewhitt said:
If there was significant viral activity all the time that would surely have been picked up by now, and though we perhaps need more investigation I suspect viral reactivation during PEM or during an ME relapse in those that experience relapses would also have been found.
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IMO, this may be the crux of the matter, the pivot point around which the debate spins. Can we trust the diagnostic metrics that historically have been brought to bear?
 
Yeah, I think there is a strong possibility that for at least a subset of patients there's something like that going on. I've had EBV as regular bloodwork before getting my M.E. diagnosis showed low levels of it in the blood, whether active or inactive. Regular screening also revealed bartonella, when googling it the "stretch-marks" on my thighs finally made sense. I've had several tests for borrelia done and most of them showed up positive.
 
I think it is unlikely that ME/CFS is caused by a persistent viral or bacterial infection, but that we shouldn’t completely rule this possibility out. IMO, the most likely explanation is that an initial infection or other trigger starts a pathway, which is perpetuated independently of the trigger.
 
Andy said:
My only beliefs about ongoing ME/CFS and LC are that they are not caused by psychological factors, and that hypotheses such as viral persistence need adequately investigating to either prove or disprove them.
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Viral persistence is possibly the longest standing hypothesis for ME/CFS and, generally, post-acute infection syndromes. Proponents argue that it may only be happening in tissues such that a blood draw would not be able to detect it. I am personally not endeared to this hypothesis, but the only certainty that we have is that it has not been properly investigated so far, in part due to the difficulty of sampling tissues. It ought to be, so that we can either pursue this lead or put it to rest once and for all.

Thus, as weary as I am of Amy Proal’s involvement with PolyBio, I am glad to see that they have been able to secure substantial funding to look at viral persistence in long Covid given that their study protocol seems quite robust.
 
With immune tolerance, in theory, virus can persist without producing antibodies, so it's only through PCR or direct culture that we can "see" them, and if they're recused in reservoirs hard to access - like brain tissue -persistence can be difficult to demonstrate.
 
Doesn't viral persistence offer a pretty good explanation for delayed PEM? Exertion and repair from that exertion take energy away from the immune system [Edit: "energy stealing" doesn't have to be the reason, could be some other unknown mechanism where exertion allows a virus to proliferate. Maybe even a mechanism that is specific to ME.], so the virus gets a chance to break out of containment and build up its levels. Replication can take a few days, as can be seen with normal acute infections.

There have been multiple studies showing RNA of SARS-CoV-2 months or years after infection in LC, but as far as I know, no evidence of the actual virus, though. But maybe it's not viral persistence of the COVID virus, but instead the proposed reactivation of other viruses, like EBV. Though it'd be much more satisfyingly simple if it was just COVID persistence that we haven't found yet.
 
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I don't think you can take energy away from the immune system in any meaningful sense. If anything repair signals would activate cells.

There seems to be pretty good negative evidence for persistence of any initiating microbe in ME/CFS. Also there is no good evidence for reactivation of specific viruses like EBV. I think it is possible that there is reactivation of immune responses to viruses or bacteria that we have raging around all the time.
 
Jonathan Edwards said:
There seems to be pretty good negative evidence for persistence of any initiating microbe in ME/CFS.
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I'm not sure how meaningful this is. Put another way, this is about as meaningful as claiming there is pretty good negative evidence for persistence of Borrelia, Babesia, or Bartonella in ME/CFS - which is not very meaningful.
 
Jonathan Edwards said:
I don't think you can take energy away from the immune system in any meaningful sense.
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That's a bit surprising to me. I just found this:

The open window of susceptibility to infection after acute exercise in healthy young male elite athletes, Kakanis et al, 2010
Abstract

The 'open window' theory is characterised by short term suppression of the immune system following an acute bout of endurance exercise. This window of opportunity may allow for an increase in susceptibility to upper respiratory illness (URI). Many studies have indicated a decrease in immune function in response to exercise. However many studies do not indicate changes in immune function past 2 hours after the completion of exercise, consequently failing to determine whether these immune cells numbers, or importantly their function, return to resting levels before the start of another bout of exercise. Ten male 'A' grade cyclists (age 24.2 +/- 5.3 years; body mass 73.8 +/- 6.5 kg; VO2peak 65.9 +/- 7.1 mL x kg(-1) x min(-1)) exercised for two hours at 90% of their second ventilatory threshold. Blood samples were collected pre-, immediately post-, 2 hours, 4 hours, 6 hours, 8 hours, and 24 hours post-exercise. Immune variables examined included total leukocyte counts, neutrophil function (oxidative burst and phagocytic function), lymphocyte subset counts (CD4+, CD8+, and CD16+/56+), natural killer cell activity (NKCA), and NK phenotypes (CD56dimCD16+, and CD56(bright)CD16-). There was a significant increase in total lymphocyte numbers from pre-, to immediately post-exercise (p < 0.01), followed by a significant decrease at 2 hours post-exercise (p < 0.001). CD4+ T-cell counts significantly increased from pre-exercise, to 4 hours post- (p < 0.05), and 6 hours post-exercise (p < 0.01). However NK (CD16+/56+) cell numbers decreased significantly from pre-exercise to 4 h post-exercise (p < 0.05), to 6 h post-exercise (p < 0.05), and to 8 h post-exercise (p < 0.01O). In contrast, CD56(bright)CD16- NK cell counts significantly increased from pre-exercise to immediately post-exercise (p < 0.01). Neutrophil oxidative burst activity did not significantly change in response to exercise, while neutrophil cell counts significantly increased from pre-exercise, to immediately postexercise (p < 0.05), and 2 hours post-exercise (p < 0.01), and remained significantly above pre-exercise levels to 8 hours post-exercise (p < 0.01). Neutrophil phagocytic function significantly decreased from 2 hours post-exercise, to 6 hours post- (p < 0.05), and 24 hours post-exercise (p < 0.05). Finally, eosinophil cell counts significantly increased from 2 hours post to 6 hours post- (p < 0.05), and 8 hours post-exercise (p < 0.05). This is the first study to show changes in immunological variables up to 8 hours post-exercise, including significant NK cell suppression, NK cell phenotype changes, a significant increase in total lymphocyte counts, and a significant increase in eosinophil cell counts all at 8 hours post-exercise. Suppression of total lymphocyte counts, NK cell counts and neutrophil phagocytic function following exercise may be important in the increased rate of URI in response to regular intense endurance training.
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So even if it's not necessarily "taking energy away", it looks like there are lots of significant changes to the immune system after exercise that might create conditions for a virus to replicate in pwME for some reason.

Though apparently there are "debunkers" of this "open window" hypothesis:

Debunking the Myth of Exercise-Induced Immune Suppression: Redefining the Impact of Exercise on Immunological Health Across the Lifespan, Campbell, 16 Apr 2018
Indeed, to this day, it is perceived by many that a vigorous bout of exercise can temporarily suppress immune function. In the first part of this review, we deconstruct the key pillars which lay the foundation to this theory—referred to as the “open window” hypothesis—and highlight that: (i) limited reliable evidence exists to support the claim that vigorous exercise heightens risk of opportunistic infections; (ii) purported changes to mucosal immunity, namely salivary IgA levels, after exercise do not signpost a period of immune suppression; and (iii) the dramatic reductions to lymphocyte numbers and function 1–2 h after exercise reflects a transient and time-dependent redistribution of immune cells to peripheral tissues, resulting in a heightened state of immune surveillance and immune regulation, as opposed to immune suppression.
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Taken together, evidence that participation in an acute bout of vigorous exercise leads to heightened infection incidence remains spurious. If symptoms of URTI are observed after a bout of vigorous exercise, the cause is unlikely to be infectious. However, if infection or immune impairment is confirmed, their trigger is more likely to be the physical, nutritional, and psychological wellbeing of the individual prior to undertaking the single bout of acute vigorous exercise. In the context of mass participation sporting events, it is likely that increased exposure to pathogens, or the influence of environmental factors that can affect immune function (e.g., travel, sleep disruption) most likely explain genuine infections. Thus, we conclude that it is unlikely that vigorous and prolonged exercise heighten the risk of infections and should not be considered a deterrent to those seeking to become more physically active.
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This seems to be a debate of sorts between the two camps:

Can exercise affect immune function to increase susceptibility to infection?, 2020

Surprisingly, I can't find any studies about duration of a pathogenic illness vs. how much bed rest/exercise a person got. I think I just don't know where to look, because I can't believe no one's looked at that.
 
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