NIH: Accelerating Research on ME/CFS meeting, 4th and 5th April 2019

Eventually.....eventually the sun's going to be a dark cinder. Hopefully before that.

 

Immunologist Derya Unutmaz, MD, who heads the NIH-funded Jackson Laboratory, has found immune system disturbances in deidentified cell samples from patients with ME/CFS, particularly in CD8 cells and T-helper 17 cells, which are involved in tissue inflammation. While emphasizing that the precise relevance of the findings is not yet clear, Unutmaz told Medscape Medical News, "There are some really major perturbations.... When I look at the data, there's something biologically terribly wrong with these people. I studied HIV for many years. This is the type of thing you would see in HIV-infected people."

Judging by the level of disability caused by the illness, there must be a fairly serious problem, albeit one that doesn't usually kill.

 

One possible reason this problem hasn't been figured out yet is that we either lack the technology or that everyone is looking at it from the wrong angle. Maybe the illness is nothing like the other illnesses that are known to exist and that's why approaching it like one of these other illnesses doesn't work.

 

Dear strategist,
I agree with your two posts. I have been worried that not enough brilliant immunologists are on the teams looking at this. And this disease will need brilliant minds, the sort that worked on AIDS.

I have no medical background, I just observe our family member. It is clear to me that there is a problem with the immune system. Our family member suffered from countless colds, strep throats, and bronchitis infections during adolescence. Most of the examinations she wrote during high school were done whilst sniffling or being on antibiotics. I would not have managed what she did.

Is it possible that folks with this are born with an immune system that is in some way already affected? And then when challenges hit the person later on in life, the system just cannot fight off viruses, infections, etc. In her case, it was after a systemic post surgical infection, and then C-difficile that the system totally collapsed. This would suggest, the immune system could no longer handle things. I really do not know, obviously.

But you raise important points. If it is on hand, would you mind very much, posting the link to Unutmaz. Thank you.

 

It's from the article posted on the previous page https://www.medscape.com/viewarticle/911906#vp_1

 

"Something in the blood"

Moderator note: Simon's summary of what we know so far about the "something in our blood" has been relocated to this thread, https://www.s4me.info/threads/blog-summary-so-far-of-something-in-the-blood-by-simon-mcgrath.9168/

 

or we are not looking at the whole picture

 

This is definitely something to look for. I read that your family member had all of these infections during adolescence and i do not know whether this is typical for a PwME. I feel that we do not know -of course this might just be me- basic things like the one you mentioned. Do PwME were getting less infections prior to ME or not? What are the actual numbers?

 

It appears that the thing they've been doing wrong is looking for the right things (microRNA's etc) in the wrong place i.e. blood serum/plasma rather than in the exosomes in the blood serum/plasma.
To be fair to NIH, they gave a grant to James Baraniuk in 2015 to look at microRNA's in exosomes in ME [https://www.healthrising.org/blog/2015/08/23/lipkin-nih-grants-chronic-fatigue-syndrome-2015/]; however, nothing was published from that study. Was the study done/money refunded to NIH?

NIH have now funded Hanson to look at microRNA's. Also, Bhupesh Prusty highlighted the microRNA's your looking for i.e. microRNA's which fragment mitochondria - he even gives the structure in his talk + José Montoya asks a question at the end of the talk highlighting the structure of the microRNA's which fragment mitochondria ("C-C-C" or something similar is common to them all).

Just Google something like "mass spectrometry + microRNA + exosome" and you'll see a bunch of stuff on how to identify/quantify microRNAs in exosomes.

I don't think we need something new here. It looks like we need to use the existing knowledge, and skills, to figure out whether ME is in effect fragmentation of mitochondria and if this is caused by microRNAs in exosomes? I.e. test Bhupesh Prusty's idea.

Bhupesh Prusty highlights that bacteria also probably have/use the same tool (mitochondrial fragmentation) to evade the immune system - sounds like Lyme disease to me.

SS-31 is a potential treatment for ME - check out Ron Davis's talk (it's the one after Bhupesh's). SS-31 has just completed a Phase 3 trial for use in a (genertic) mitochondrial disease - so it's presumably a candidate for re-purposing for use in ME.

If your in the UK/Europe there's an European Union (EU) Election next month - try working with ME Action/Millions Missing groups. E.g. to ask your outgoing Member of the European Parliament (MEP) why the EU has given 33.9 million euros to Lyme disease research (last 10 years) and zero to ME. Lyme effects approx 1 million people in the EU; ME effects approximately 2 million.

@Esperanza @JaimeS @EspeMor @Perrier

 

not sure, but thought this might be relevant/of interest

The study “GM-CSF and CXCR4 define a T helper cell signature in multiple sclerosis” was published in the journal Nature Medicine.

article here:
https://multiplesclerosisnewstoday....s-patients-may-cause-inflammation-study-says/

 

all individual presentations available on Youtube:
NIH 2019 Conference: Accelerating Research on Myalgic Encephalomyelitis & Chronic Fatigue Syndrome
12 videos Updated yesterday

https://www.youtube.com/playlist?list=PL9KL7sas9xFnfRU_o8V7gQGaCTYVjW9mX

 

MEAction have uploaded 29 individual videos to their channel as well
https://twitter.com/user/status/1178361355587506176


https://www.youtube.com/playlist?list=PLhO4nWkiP5QRt_Hjd4B-PWpKMlIJxXXrM