ME/CFS as a hyper-regulated immune system driven by an interplay between regulatory T cells & chronic human herpesvirus infections (2019) Nacul et al.

Interesting, this appears to be more specifically about what I have which is comforting to see.

Makes me glad I backed the LSHTM biobank.

ME specialists from CureME, apparently working on an NIH project.

https://me-pedia.org/wiki/CureME

My thanks to them all.

 

Are they saying my herpes simplex virus does more than occasionally give me cold sores in the face?

 

Autoimmunity and chronic viral infections are recurrent clinical observations in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), a complex disease with an unknown cause.

That statement seems a bad place to start. I am not aware of any basis for it.

 

I am, that fits my CFIDS symptoms to a tee.

 

Yes as you pointed out recently there's no strong evidence for B-cell autoimmunity (rituximab failure) and not much for T-cell autoimmunity. So that just leaves chronic viral infections and so far studies looking for virus's haven't been finding much (Ron Davis etc. however he's only really covered one class of virus's - viral DNA, or RNA, but I can't remember which).

 

It might be autoimmunity after all. Then again, it might not be... At the end of the day we are still clueless after 40 years of research. I doubt that there's many other illnesses where research has been so incredibly unfruitful.

 

It'd be useful to see the final paper, I think. I presume/hope the hypothesis is based on actual findings at the Biobank, rather than wild guesses.

Then we'd be able to see what basis there is for this theory and how likely it is to be right. Only time will tell.

 

They must be aware of the Rituximab results, agree will be interested to see what the full paper is saying.

I am just "delighted" they are looking at chronic viral infection as a characteristic symptom of ME.

https://www.meassociation.org.uk/20...-to-improve-symptoms-in-me-cfs-03-april-2019/

I am pushed to understand how else I would get palindromic rheumatic pain in symmetrical patterns shifting through my joints over a number of years other than by an autoimmune reaction. If the people in the large Rituximab trial did not experience a relief of symptoms then it seems plausible to me we do not have the same illness.

Though the 150 patient Rituximab trial used Canadian Consensus Criteria, CCC cohorts can include people with zero immune deficits, potentially different subtypes if not diseases from CFIDS. I honestly think we may have an apples and oranges problem.

Besides which there is more to HHVs since they (egEBV) produce their own cytokines (IL10) which could do something similar in terms of turning down the immune response without invoking autoimmunity.

 

Unfortunately, that 40 years of research has had about as much funding as 1 year of MS research (maybe more but definitely not much) and much of that research has not actually been on ME but on fatigue states which may not be relevant.

Also the patients being tested have been a rag tag bunch who may not have had ME in the first place because of the lax definitions used.

It is hopeful in the sense that the cause of ME may not be any harder to find than any other disease if money and attention are focused in the right places.

 

I have a feeling that this is a theoretical modelling paper, not a data based paper.
I am not aware of any data to go with it.

 

My information is that the Biobank team have found some differences in mucosa-associated invariant T cells (MAIT) but not T regs.

 

I agree.

 

Alzheimer's https://www.healthrising.org/blog/2019/09/16/alzheimers-chronic-fatigue-fibromyalgia/?

Lyme - http://simmaronresearch.com/2019/10/better-lyme-diagnostic-nih-strategic-plan/
A lot of money has been spent on a diagnostic test and it hasn't been delivered yet ---- post Lyme disease could be ME of course!

 

It would also be interesting to know the length of time these patients have been ill. My immune system has morphed over 30 years.

 

The full paper is out now (free access): Link

 

Bump.
Looks like it's a mathematical modelling paper.
Above my head. What, in a nutshell and in plain English, does it say? And what relevance/implications does whatever it says have?

 

All above my head too and I couldn't be bothered trying to understand it.

None of the following may be relevant to the theory presented in this paper!

I think one of the problems with the active virus theory is that Ron Davis etc. can't find viral DNA (not much done on RNA virus's yet). To be fair the same problem seems to occur in Lyme i.e. a lot of people considered to have with Lyme do not test positive http://simmaronresearch.com/2019/10/better-lyme-diagnostic-nih-strategic-plan/

So it seems we need a theory to explain these negative tests and a pathogen theory.

I think Bupesh Prusty is preparing a publication at the moment so here's hoping that this will help explain how we get from no detectable pathogen to ME.

There seemed to a reasonable model [of a post infection fatigue type illness] presented at the EMERGE Conference (Feb 2019?) re a disease which affects people living near intensive goat farms in the low countries (Neherlands?). From memory the idea is that bacteria persist in bone marrow for years - maintaining the immune response.