Is there good evidence that ME/whatever after an enteroviral infection is very different to states after other infections?

Some people insist ME can only follow from an enterovirus; there are other post viral/infectious sequelae but they are distinctly different and not ME.

I don’t recall reading about any studies that showed this but I don’t know or recall every bit of evidence of course.

 

There is a list of studies here: https://me-pedia.org/wiki/List_of_enterovirus_infection_studies

It's strange how little mention the enterovirus in tissue studies get. On the surface, the studies seem interesting and convincing. Why aren't scientists trying to replicate this?

PS: I now see that some replication attempts were made with negative results.

 

Even if we assume ME is caused by an Enterovirus, Enteroviruses are really common so i don't see why they wouldn't be able to sneak in while the immune system is busy fighting another major infection.

 

After the 1990s ME had become CFS which had a much wider definition. It was also so unspecific that it was possible to cherry pick patients so the negative results found by the psychologists at the Nijmegen Group in the Netherlands is not surprising.

The whole sociology, if that is the right term, of enteroviruses is fascinating. There is this whole myth that only polio was dangerous and that has been conquered so the rest are common and mild infections so not worth bothering about.

But serious enteroviral disease still exists. Acute Flaccid Myelitis (called acute flaccid paralysis in the US) still comes in epidemics and is very similar to polio, yet the CDC denied it was enteroviral for a long time, claiming that everyone has antibodies to enterovirus.

I was at a talk by John Gow and he did not seem to realise that polio was a simple respiratory disease in most people who got it, with only a few developing classic polio. If ME is caused by an enterovirus then it is only a few people who get infected who go on to get ME.

Enteroviruses are still difficult and labour intensive to detect. PCR only looks for enteroviral RNA but that is like looking for the presence of coronavirus without checking for SARS-CoV-2. It is useful for acute infection but not for ME studies.

Though they are wonderful viruses with all sorts of tricks to avoid the immune system. Since viruses only use energy for what is useful, dropping things that are no longer necessary to them, it is hard to see why they have these abilities unless it is to let them persist after acute infection.

The evidence indicates that enteroviral ME exists and accounts for many patients.

 

Looking at the MEpedia page my impression is that we do not have any reliable evidence for enteroviruses being involved in ME. I suspect there was a pre-existing theory that they would be found and so a variety of studies published weak evidence to support that. The tissue staining studies do not look to me to be significant. Artefacts are very common with the technique used. Antibody titres do not tell us anything useful generally speaking.

If specific viruses played a special role we would expect ME/CFS to be a much more obviously epidemic illness. The more I see of the few so-called ME epidemics the less I think they tell us about the condition in general.

 

ME may be caused by other viruses and bacteria, but enterovirus is one of them and that aspect is dreadfully under researched compared with herpesviruses.

 

To be honest, I'm a bit puzzled by the continuing focus on viruses in some ME research. Given that there have long been reasonable grounds to suspect several different triggers, is it useful to put resources into defining exactly what they are until we're further along with research?

It doesn't help us much with diagnosis – EBV being a possible exception. It doesn't appear to help with treatment either, as doctors have tried strategies aimed at tackling various types of underlying infection, with mostly unconvincing results. And it's impractical to prevent people coming into contact with the viruses under suspicion.

It seems much more important to gain some understanding of what happens in the body after the precipitating event(s), what perpetuates that state, and whether some people are more susceptible. It's entirely possible that we could find strategies that improve symptoms, years (if not decades) before we can say anything definitive about triggers. I get the impression that this has been the way research into some other chronic conditions has panned out.