Latent viruses as a cause of ME/CFS

I had mono before ME/CFS. A few years ago a naturopath got me to do a blood test at Armin Labs in Germany to test my 'EBV status.' The results apparently indicated "humoral immune response against Epstein Barr Virus (chronic or reactivated or EBV-infection in convalescence?" [sic]. I attached the relevant pages from the lab results with my name redacted.

She recommended I do 'micro-immunotherapy' using a supplement called 2LEBV from a company called Labo'life. The product was very expensive and it made me feel significantly worse the entire time I was taking it. Just thought I would share my experience in case it's relevant.
 

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PageofME said:
I think my reply was adequate.
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Your reply was nonsensical, since you were refuting a claim which wasn't made.

As is your present reply, since SugarSquared didn't specify anything about herpesvirus or lytic state.
PageofME said:
that explains why when @SugarSquared asked about the illnesses that herpesviruses cause in the lytic state
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SugarSquared said:
Just throwing a question out there, but are there any illnesses caused by latent viruses? It would be useful to be able to compare.
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Can we infer anything from the results of various immune-modulating/suppressive trials? Rituximab, Daratumumab, Immuno-adsorption, Rapamycin come to mind.

Would we expect patients to get (much) worse from such treatments?

Would lowering antibody levels even have substantial impact on the immune system of the brain (assuming that where viruses could "hide")?

Edit: And of course steroids. There was a Charité trial of Methylprednisolone, which penetrates into the brain. But all I know is that it was aborted due to serious side-effects. Terrible headaches that lead to hospitalizations, if I recall correctly, so maybe a side effect of the relatively high dose.
 
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Is the term smoldering infection a thing in medicine? I'm intrigued by the off-switching of itaconate where our body's own anti-inflammatory responses deployed for protection can become part of why our immune system stays "stuck' and why latent infections reemerges.

This is why I'll never take immune modulators ever again that reactivated all herpes viruses at one time years ago.

I feel like I'm stuck in a loop.
 
fst said:
Can we infer anything from the results of various immune-modulating/suppressive trials? Rituximab, Daratumumab, Immuno-adsorption, Rapamycin come to mind.
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I don't think we can infer anything very solid. Rituximab therapy is not associated with increased problems from hidden viruses very often. There have been some very rare cases of JC virus related leucoencephalopathy but nearly all in people who had another source of immune deficiency as well as being given rituximab.

Shingles does occur quite often after rituximab though, so for herpes viruses your argument is relevant. We might at least expect some people to get worse if ME/CFS was dependent on low grade herpes viral effects. One or two people have reported being worse but not many in the Norwegian trials got worse.
 
A small CFS trial of 36 patients taking Immunovir in the late nineties helped improve their 'fatigue', they felt less tired. I had a terrible relapse after only 3 weeks on the medication when I was feeling 90% better before that.
 
fst said:
Can we infer anything from the results of various immune-modulating/suppressive trials? Rituximab, Daratumumab, Immuno-adsorption, Rapamycin come to mind.

Would we expect patients to get (much) worse from such treatments?

Would lowering antibody levels even have substantial impact on the immune system of the brain (assuming that where viruses could "hide")?

Edit: And of course steroids. There was a Charité trial of Methylprednisolone, which penetrates into the brain. But all I know is that it was aborted due to serious side-effects. Terrible headaches that lead to hospitalizations, if I recall correctly, so maybe a side effect of the relatively high dose.
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If you read anecdotes about rapamycine many actually DO feel worse while on it, although of course the dose is much lower than normally used for immunosupression.

Also there definitely are people that feel worse after immunoadsorption, temporarily or permanently, as well as some prominent cases (Whitney Dafoe, Olaf Bodden) who got significantly worse after rituximab.

But I don't think you could seriously deduct anything about the role of herpesviruses in ME from any of this as of course worsening could have happened through various side-effects or through the extertion alone.
 
MrMagoo said:
I wish we had like a Google earth map of theories, I could zoom in on a body part and down to cells into what it is and what it does and what the theory is
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I get you. However, in my view research into herpes theories is the only one that actually continually delivers results. The rest is just specualation that isn't leading anywhere yet. So it's all not so complicated.
 
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An important drug discussion related to herpes theories is in our thread on acyclovir/valacyclovir/famciclovir.

Truvada is also interesting. All these meds have activity against early phase EBV reactivation which is currently the best explanation why they seem to work continually for a subgroup of ME/CFS patients.
 
Creekside said:
Yes, my first experience of ME was feeling exactly like I was coming down with a flu ... except that the symptoms were gone the next day, which is not the pattern for a viral infection. We have symptoms that are produced by internal mechanisms that can be triggered by viral infections, but that doesn't mean that they're the only possible trigger.
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It might be the pattern of abortive-lytic herpes reactivation. Regarding initial triggers, I think the consensus has been for a long time that it's often viruses but can be other things that can damage or temporarily incapacitate the immune system like chronic distress, trauma (surgery, accidents), ect.
 
Silip said:
If you read anecdotes about rapamycine many actually DO feel worse while on it, although of course the dose is much lower than normally used for immunosupression.

Also there definitely are people that feel worse after immunoadsorption, temporarily or permanently, as well as some prominent cases (Whitney Dafoe, Olaf Bodden) who got significantly worse after rituximab.

But I don't think you could seriously deduct anything about the role of herpesviruses in ME from any of this as of course worsening could have happened through various side-effects or through the extertion alone.
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Looking at the trials, I think it is safe to say that the majority of patients does not feel considerably worse after those treatments.

But as JE pointed out, it we can't expect these treatments to (consistently) reactivate viruses in the first place, so yes, the idea is a dead end.
 
PageofME said:
An important drug discussion related to herpes theories is in our thread on acyclovir/valacyclovir/famciclovir.

Truvada is also interesting. All these meds have activity against early phase EBV reactivation which is currently the best explanation why they seem to work continually for a subgroup of ME/CFS patients.
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But do they? If EBV reactiviation would be the sole culprit of some ME and these drugs work as well as you claim it, we would see hundreds of people getting in remission through them every year.

I know of dozens of people who have tried the Lerner protocol with (val-)aciclovir, and I heard of 1 single person who got in remission, this person had strong hints for repeated/ongoing herpes zoster reactivations.

Some others claimed minor benefits, but, even when not taking in the chance that this is placebo and/or improvements occured naturally over those month that they took antivirals, just minor benefits would at least mean that
a) reactivated herpesviruses are only a part of what causes ME or rather consequence than cause
and/or b) these drugs don't work very well against EBV in-vivo; either because they don't supress reactivation well enough or because they can't reach the site where reactivation is happening

You can't claim both, that these drugs are really effective in treating EBV-reactivation in ME AND that EBV-reactivation is the sole culprit for ME for a significant group.

I'm definitely interested in theories related to herpesviruses, but tbh your claims about the effectiveness of these antivirals for ME make it hard for me to take your arguments seriously.
 
PageofME said:
Truvada is also interesting. All these meds have activity against early phase EBV reactivation which is currently the best explanation why they seem to work continually for a subgroup of ME/CFS patients.
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The best drug for hitting EBV that I know of is rituximab. Dorothy Crawford is probably the chief EBV authority in the UK now (she worked with my mother years ago at the Central Public Health Lab, Colindale). I am pretty sure she published that you can eradicate EBV in peopple with EBV-dependent neoplasia with rituximab.

Why does rituximab have no effect on ME/CFS if EBV is an active mediator?
 
The virologist I saw was a physician-scientist and clinical researcher, he saw many pwME/CFS. Some of his patients recovered from taking medications, but my impression was that the patients who recovered were put on meds early in the illness. I don't know if they actually had ME/CFS, or that by taking meds early prevented them from worsening into ME/CFS.

My personal opinion is that ME/CFS from day one is already in the cards, possibly genetics.
 
Jonathan Edwards said:
The best drug for hitting EBV that I know of is rituximab. Dorothy Crawford is probably the chief EBV authority in the UK now (she worked with my mother years ago at the Central Public Health Lab, Colindale). I am pretty sure she published that you can eradicate EBV in peopple with EBV-dependent neoplasia with rituximab.

Why does rituximab have no effect on ME/CFS if EBV is an active mediator?
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Check out Michela Locci's latest UPenn/PolyBio work (as highlighted by Amy Proal during PolyBio's Spring 2026 webinar on YouTube) using fine needle aspirates—she found dysregulated germinal center B cells (and potential EBV reactivation) exclusively inside lymph nodes, not in peripheral blood. If the pathology is localized to tissue, it might explain why the rituximab trial didn't pan out.

(Also, EBV might not be the only virus that gets reactivated. I have a friend with ME/CFS who is EBV negative. Next to an LC group with EBV reactivation, VZV has popped up recently as another possible candidate in Mark Painter's work (a T-cell specialist also at UPenn) which he presented in the same webinar as mentioned above)
 
PageofME said:
Check out Michela Locci's latest UPenn/PolyBio work (as highlighted by Amy Proal during PolyBio's Spring 2026 webinar on YouTube) using fine needle aspirates—she found dysregulated germinal center B cells (and potential EBV reactivation) exclusively inside lymph nodes, not in peripheral blood. If the pathology is localized to tissue, it might explain why the rituximab trial didn't pan out.
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Not if Dorothy's work is valid. We have known all along that rituximab does not clear all B cells, and in particular it does not ablate follicles. But it seems to be able to eradicate EBV. It may be that EBV infected B cells have a different pattern of survival ligands expressed and are all ritux sensitive.

The failure of rituximab to help ME/CFS is unlikely to be due to persistence of B cells in follicles. Vaccination studies suggest that while rituximab is there you cannot mount a new antibody response to a vaccine. Rituximab seems to be very good at stopping the formation of new antibody but it does not act directly on the production of antibody from long lived plasma cells. The likeliest explanation for the trial failure is of course that antibodies are not involved in ME/CFS. The second most likely is that, as for several autoimmue diseases, relevant antibodies are long-lived plama cell derived.
 
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Jonathan Edwards said:
Not if Dorothy's work is valid. We have known al along that rituximab does not clear all B cells, and in particular it does not ablate follicles. But it seems to be able to eradicate EBV. It may be that EBV infected B cells have a different pattern of survival ligands expressed and are all ritux sensitive.
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Or maybe not...

Why don't you have a look at what they're doing at UPenn. You probably understand better than anyone else here what they're up to and could explain the details to us.
 
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