Revisited - Does ME/CFS more closely resemble an autoimmune disease or a chronic infection?

[halcyon]

I have not heard of the VP1 antigen test mentioned in that study (it sounds like they detect antibodies to the enterovirus VP1 capsid protein).

However, note that this is not the same as the VP1 staining of biopsied tissues, which is the method Dr Chia uses to detect enterovirus infections in stomach tissue biopsies.

Both methods use the same 5-D8/1 monoclonal mouse anti-VP1 antibody. It's not outlined in the study linked, but I presume they used Mowbray's method (or perhaps even Mowbray's lab performed the assays), which was a western blot of serum looking for enterovirus VP protein bound to the added 5-D8/1. Chia starts with the same 5-D8/1 antibody and then does an immunoperoxidase method, on tissue of course instead of blood.

 

[halcyon]

Elderly people have encountered many infections in their lifetime and have antibodies to them.

They are also often sedentary. It's well known that enterovirus infection + activity = worse outcome and Ramsay and Dowsett remarked that those that rested from the beginning infection stage had better outcomes.

 

[halcyon]

In my opinion, one of the most interesting papers is the one that describes a Giardia outbreak in Norway and follows the patients that developed ME afterwrds.
Giardia causes ME? Or is it just a triggering event?

....brain fog.....

Reading case descriptions of the first outbreaks is interesting, it seems that the clinical evolution of those cases resembles more of a acute encephalytis than a chronic imune disfunction, maybe the virulence of the infectious agente has changed..

This outbreak is interesting to me too but not because of the Giardia, which of course doesn't cause encephalomyelitis. The victims were exposed to the Giardia via sewage contaminated drinking water, which almost certainly was ripe with huge amounts of enterovirus as well.

 

[halcyon]

Why is Dr Chia sort of on the sidelines? A few years ago on the telephone he told me virtually all his patients with CFS were positive for enterovirus.

His clinic will be one of three collaborating with Maureen Hanson's newly funded center.

 

[Groggy Doggy]

You might be right that to an extent, patients with active enterovirus infections may tend to go to Dr Chia. However, I would guess that most of his patients don't know in advance whether they have active enterovirus infections or not, because testing for enterovirus can only be done using expensive specialist tests available at only only two labs in the US.

And in Dr Chia's published letter, out of 200 consecutive patients that came to his office, he found 54.5% had their ME/CFS attributable to enterovirus.


Where were you tested for coxsackievirus B and echovirus, by the way? If it was not done at a lab that uses the antibody neutralization method (used by ARUP Lab and Cambridge Biomedical), or by Chis'a stomach biopsy testing, then your negative test results are useless and don't mean anything. The only blood test method that is sensitive enough to reliably detect chronic enterovirus infections is the antibody neutralization method.

Tests done by the very best: ARUP Labs, Salt Lake City, Utah

 

[TreePerson]

Average age of onset appears to be around menopause. Its most often women in their 40s. However it hits both sexes and all ages. Its hard to judge about older people though, because if they were susceptible they probably got it at a younger age.

I got it in my head that the average age of onset was 35. Typically the menopause is 50 to 52. I don't get the impression that most women acquire the disease during the menopause. In fact I can't think of a single person I've seen online where that's been the case.
I do agree that susceptible people will probably have succumbed well before old age.

 

[Mithriel]

Just some thoughts reading this interesting thread.

Channelopathies as a cause is another interesting lead that just petered out. I can't remember the name of the Hawaiian researcher who did all the work but he died and no one I know of carried it on. He found an anti ciguatera toxin or something and the NIH did work on the same thing but called it something else so nothing quite came together. I can't remember very well today It seemed really promising and I hope it is still being looked at.

The early thinking was that the people who got ME were ones who came into contact with a lot of infections but who were least able to rest when they got ill. I am not sure if cancer survivors actually get ME with the broken aerobic system. It is more likely they get a post cancer syndrome with chronic fatigue. The strong chemicals and radiation must put a terrible strain on their bodies. It may be the same as ME but we would need to do 2 day CPET testing to find out. In fact it would be interesting to do testing on people with different onsets.

There have been many different common viruses given as triggers for MS, but the real question is how they cross the blood brain barrier which is designed to keep them out. Their was a fad for raspberry extract for a while which is meant to strengthen it. The immune system doesn't work in the brain so how does the autoimmunity affect it?

That may be important for us with mircroglial involvement and so on. If we could lift the brain out and look at it it would be so much better!

There should not have been virus present in the brain at autopsy. After the Gulf War they found that stress caused the barrier to break down which could explain why MS people seem to have stressful events before major relapses.

I do not know if it is just common knowledge, but in a throwaway line in an ME article years ago (about stealth viruses I think) they mentioned that the immune system components are made of viral particles. I do not know if it is true or important but it does mean that any virus could cause autoimmunity.

 

[Galixie]

My brain is not cooperating lately, but after reading @Woolie's comment about auto-inflammatory diseases I hopped over to google to find out what that was and I found this page, which helped un-confuse me a bit: http://saidsupport.org/autoinflammatory-vs-autoimmune-what-is-the-difference/

I find the autoinflammation idea interesting. I've been hesitant to view my issue as autoimmune specifically because I don't see any evidence that my immune system is actively attacking any part of me. But autoinflammation does sound more like what I'm dealing with. Except that I don't get recurring fevers. I wonder how important that symptom is? Hmm.

 

[Jesse2233]

@duncan @Galixie

are treatments used for autoinflammatory conditions similar to those used for autoimmunity?

for example if B-cells (as well as T-cells) are producing pro-inflammatory cytokines, then benefit from rituximab (or other immune suppressors) might still make sense right?

 

[Woolie]

@duncan @Galixie

are treatments used for autoinflammatory conditions similar to those used for autoimmunity?

for example if B-cells (as well as T-cells) are producing pro-inflammatory cytokines, then benefit from rituximab (or other immune suppressors) might still make sense right?

No, they different. They're things that work by inhibiting the production of key inflammatory cytokines, drugs like etanercept (inhibits tumour necrosis factor) and anakinra (inhibits IL1). There's also the hugely expensive monoclonal antibody drug canakinumab, which inhibits IL1.

Some of these are used for autoimmune disorders too.

I found this page, which helped un-confuse me a bit: http://saidsupport.org/autoinflammatory-vs-autoimmune-what-is-the-difference/

@Galixie's link is really helpful.

I only know about these diseases because I'm suspected of having one (will post more if that's confirmed). They are rare, apparently, but I do wonder if that might be because no-one knows about them so they mostly go undetected.

 

[duncan]

They are different still for channelopathies, where frequently the best that can be offered is to try to mitigate downstream effects like life-threatening cardiac issues with beta blockers or whatever.

ETA: It is also true that depending on the brand of channelopathy, partial treatment can be attempted with supplements or thru diet, especially if levels (eg potassium or sodium) can be determined during episodes. But even these treatments are frequently at best marginal.

 

[Woolie]

Except that I don't get recurring fevers. I wonder how important that symptom is?

I get recurring flu-like episodes, and during these I have raised blood markers indicative of inflammation. But my temperature doesn't go up that much. Maybe half a degree max. And I don't get rashes during episodes. For this reason, my record says "?atypical periodic fever syndrome". Its not confirmed yet, and might never be.

It has occurred to me that new diseases are discovered in people with the most extreme presentations. The sort of presentation that leaves no doubt that something is horribly wrong, and that provides lots of clues as to what the problem might be. Once a disease is better understood, milder variants might be discovered.

I think that's pretty much the history of Lupus and MS.

I'm not trying to say that ME is another auto-inflammatory disease. But it might share some similarities.

 

[fingers2022]

Is it that old people don't get the disease, or is it that it is considered as normal aging consequences for old people to suffer from pain and fatigue and cognitive dysfunctions...

I guess the second point is more likely to be right....

Nah, ME is totally different to ageing. It is lights on lights off...or it ain't the ME I know.

 

[ladycatlover]

It has occurred to me that new diseases are discovered in people with the most extreme presentations. The sort of presentation that leaves no doubt that something is horribly wrong, and that provides lots of clues as to what the problem might be.

The problem is that we have 25% with extreme ME, including within them the most extreme presentations, and most of them have no help from medical professionals of any kind at all. Not even a GP visit once a year or even once every five or ten years.