Are Infections Just a Trigger of ME/CFS, or an Ongoing Cause of ME/CFS?

[Hip]

I don't really trust a CDC statement that Parvo B19 can cause symptoms consistent with CFS - the problem there is probably one of definition.

In the case of parvovirus B19, it was not the CDC that said it can cause symptoms consistent with ME/CFS, but rather it was these studies by Jonathan Kerr et al:
Chronic fatigue syndrome and arthralgia following parvovirus B19 infection

Antibody to parvovirus B19 nonstructural protein is associated with chronic arthralgia in patients with chronic fatigue syndrome/myalgic encephalom

Detection of herpesviruses and parvovirus B19 in gastric and intestinal mucosa of chronic fatigue syndrome patients

Kerr, who was involved in ME/CFS research a few years ago, was particularly interested in parvovirus B19 because of the very fact that it can cause ME/CFS symptoms. He thought that this virus, and the cytokines it induces, would be good to study, as it might throw light on the mechanisms of ME/CFS.

I found it very interesting that Kerr showed parvovirus B19 infection induces the inflammatory cytokines IL-1β, TNF-α and IL-6, because these specific cytokines are exactly the ones that are known to cause sickness behavior, which as we know has symptoms very similar to ME/CFS. So I think the induction of sickness behavior is the likely mechanism by which parvovirus B19 causes ME/CFS.

Jonathan Kerr's study on the cytokines induced by parvovirus B19 is this one:

Cytokines in parvovirus B19 infection as an aid to understanding chronic fatigue syndrome

I think many pathogens DO trigger ME.

Another possibility that we might consider is that pathogens may initially trigger something like autoimmunity, or cause some initial hit and run damage to the body or brain, which helps set the scene for ME/CFS, and in addition, the ongoing infection also helps maintain ME/CFS.

In other words, it is not inconceivable that there may be both an initial trigger action, as well as an ongoing causal action from a chronic infection.

 

[msf]

Eeyore, re: polio, I invite you to read the blog I wrote about post-polio syndrome (or skim through it to find the papers I posted links to). Basically, it turns out that post-polio patients may indeed still be infected with polio. The evidence isn't conclusive, but while this is a possibility I think using polio as an analogy is a bit of a non-starter.

 

[Hip]

As an addendum to the IL-1β, TNF-α and IL-6 cytokines Jonathan Kerr found in parvovirus B19 infection:



The enterovirus infections of the stomach that Chia found in ME/CFS patients could easily explain ME/CFS symptoms, by the following mechanism, based on the three cytokines IL-1β, TNF-α and IL-6:

The sickness behavior state, which is induced by the inflammatory cytokines IL-1β, TNF-α and IL-6, has symptoms very similar to those of ME/CFS, and it has been proposed that ME/CFS may simply be a chronically maintained state of sickness behavior (at least in part).

We know from Jonathan Kerr's work on parvovirus B19-triggered ME/CFS symptoms detailed above that parvovirus infection induces these exact three inflammatory cytokines in the body. So that's good indication that the IL-1β, TNF-α and IL-6 may play a causal role in precipitating ME/CFS symptoms.

So now we have both an explanatory theory (the sickness behavior mechanism) and empirical evidence (Kerr's studies on parvovirus) that IL-1β, TNF-α and IL-6 may be may causing ME/CFS.

And when I checked myself on PubMed, I found that one commonality of nearly all ME/CFS-associated pathogens was the fact they all induce these particular three cytokines. Not all pathogens do this. So that is further evidence of the involvement of these cytokines in ME/CFS.


So what is so special about an enterovirus infection in the stomach? Well, the vagus nerve, which is the nerve that triggers sickness behavior when it detects the cytokine IL-1β, innervates much of the stomach. Thus, if even this low-level "smoldering" enterovirus infection of the stomach is only chronically producing small amounts of IL-1β, the close proximity of this infection to the vagus nerve may cause a significant and chronic triggering of sickness behavior.

So here you have a nice theory of how an enterovirus infection of the stomach may cause ME/CFS.

The theory is just a variation of Michael VanElzakker vagus nerve infection / sickness behavior theory of ME/CFS.


Note: the above is just duplicate of this post.

 

[msf]

Re: whether it is a trigger or an ongoing cause, I would say it's both. There isn't much evidence for either at the moment, but in my eyes the trigger theory is a bit of a non-theory. There isn't really any explanation for why some patients get better and some go on to have ME. The ongoing cause theory is simple: it's because they have failed to clear the infection. Apart from exotic and not very well-understood diseases like Dengue and Ebola, I don't know of any examples of a hit-and-run in medicine, whereas I know of lots of examples of chronic infection leading to chronic illness.

 

[msf]

One of which, according to the Dubbo study, is a cause of ME/CFS (Q fever).

 

[Hip]

I don't know of any examples of a hit-and-run in medicine

What about viral or bacterial meningitis, which only lasts for a few hours or days, but which can lead to permanent loss of mental faculties and permanent personalities changes.

 

[msf]

I don't now anything about that, but to me it sounds like that it causes permanent damage rather than a permanent disease process.

 

[Hip]

Basically, it turns out that post-polio patients may indeed still be infected with polio.

This was mentioned earlier in this post.

 

[msf]

Sorry, I didn't read all the posts.

 

[Hip]

I don't now anything about that, but to me it sounds like that it causes permanent damage rather than a permanent disease process.

In this context, "hit and run" means that an acute pathogenic infection, and/or the immune response to that infection, has caused some damage to body tissues.

 

[msf]

Oh, I thought it meant that the resulting ongoing immune process causes ongoing damage to body tissues and functions.

 

[msf]

For clarification, I doubt that those meningitis patients would have raised cytokine levels for 3 years after the episode.

 

[msf]

Anyway, it's not surprising that we don't know what theory each other is talking about, because from what I've seen no one has come up with a comprehensive theory to support to the 'hit and run' idea, with the possible exception of the Dubbo study, which as I pointed out earlier also found evidence for chronic infection causing ME.

 

[msf]

And the Dubbo example wasn't a true hit-and-run anyway, since EBV stays in the body.

 

[halcyon]

Apart from exotic and not very well-understood diseases like Dengue and Ebola, I don't know of any examples of a hit-and-run in medicine

I'm not sure ebola classifies for hit and run, evidence of persistent infection has been found in survivors after seroconversion and there does appear to be a post-ebola syndrome.

 

[msf]

That's why I said it was it was not well understood.

 

[Hip]

Anyway, it's not surprising that we don't know what theory each other is talking about,

What we are talking about in this thread was defined at the beginning of this earlier post. The meaning for the terms "trigger" and "ongoing cause" being used in this thread were spelled out there.

 

[msf]

Where? I would be surprised, because, as I said, I don't think any doctors have come up with a comprehensive theory to support the 'hit and run' idea before. And without trying to be hostile, the meningitis analogy you mentioned was a complete red herring, in my view. It is like saying that because chicken pox causes pock marks in the skin, those patients have a post-chickenpox syndrome.

 

[Hip]

Where?

Can you not see where "trigger" and "cause" are defined. Look again, in this post.

I don't think any doctors have come up with a comprehensive theory to support the 'hit and run' idea before.

The metaphorical phrase "hit and run" is not being used here as a proven theory, it is being used a description of the real or hypothetical permanent damage caused to the body during an acute infection.

Hit and run damage most definitely occurs during some infections, like meningitis, encephalitis, and influenza can cause permanent hit and run damage to the lungs. Whether such hit and run damage might occur during the acute infections that often mark the beginning of ME/CFS is one of the discussions of this thread.

If you can provide any studies that either support or refute this hit and run possibility in ME/CFS, please do so.


Some people do develop ME/CFS after an episode of meningitis, so that perhaps may be suggestive of a hit and run etiology.

 

[halcyon]

That's the problem, I'm not aware of any model that's been put forward to explain what would be happening in the hit and run model, and yet this is the model that seems to be promoted by a lot of people. I don't believe that a disease like ours with daily fluctuations in symptoms and a relapsing/remitting course can be explained by one time cellular damage. I believe it would have to be an ongoing process of cellular damage or dysfunction, provoked by either antigen or autoantibodies, or both. I'm not aware of any disease or dysfunction that is caused by the immune system "just freaking out" without any stimulus, though I don't have a background in medicine.