Key question for those knowledgeable of Drs. Naviaux's and Prusty's theories

[serg1942]

Hi everybody,

I have been catching up with Dr. Naviaux's papers, and I have also read the paper published by Naviaux, Prusty et. al on HHV-6 reactivation in ME/CFS:

https://www.immunohorizons.org/content/4/4/201

I have just listened to the recent Prusty's talk on their unpublished and most recent updates from the lab:

Here, Dr. Prusty finds that about half of ME patients show high autoantibodies against the complement protein C1q. Moreover, when these autoantibodies are added to healthy cells, they induce a CDR state (with fragmented mitochondria). So, autoantibodies against C1q could be one of the factors given off by a cell that senses a threat in order to alert the neighboring cells and force them to enter into the CDR state ("CFS cells").

This is my question: why are they looking for the "signaling factor" that would explain why serum from ME patients make healthy cells to become "CFS cells", knowing that these signaling molecules are purines (mainly ATP)? We know this because suramin reversed two murine autistic models and also greatly improved clinical symtoms/behavior in 5 autistic children after just one dose of suramin:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334917/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596371/?report=reader#!po=90.3571

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5497533/

So, I don't get it: there is an stressor that makes the mitochondria in a cell to enter into the CDR antiviral state, and then this cell sends extracellular ATP to its surrounding so that the neighboring cells sense the extra ATP and then enter into CDR as well.

Aren't then the purines the signaling factors in serum from ME what makes the healthy cells to become sick? So why are they looking for other factors? (autoantibodies anti-C1q, IgGs, beta 1 and 2 adrenergic receptors, eosinophil cationic protein).

Any help trying to figure out this point will be much appreciated!.

Thank you in advance!
Sergio

 

[jpcv]

I understand that purines are the way mitochondria "talks" to each other, but what causes the first danger signal that sets off this "danger" reaction?

 

[sometexan84]

Wanted to chime in, as I've been looking into complement dysfunction and activation for a bit now.

No answers really, but some associations...

EBV could be the cause of C1q antibodies - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6853867/

C1q antibodies are also associated w/ ...
Glomerulonephritis (GN)
Systemic lupus erythematosus
Vasculitis

I also just learned C1q antibodies are associated w/ autoimmune thyroid disease (Graves and Hashimoto's). Not only that, but C1q antibodies correlate positively to TSH in Hashi, and negatively to TSH in Graves. So, more or less, C1q is also associated w/ hypothyroidism. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2249.2008.03670.x

 

[Canned]

EBV could be the cause of C1q antibodies - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6853867/

At least, elevated c1q autoantibodies can be an indecator that ebv might be the Virus that is causing your ME. Which i think is quite a usefull Informationen in terms of treatments.

also just learned C1q antibodies are associated w/ autoimmune thyroid disease (Graves and Hashimoto's). Not only that, but C1q antibodies correlate positively to TSH in Hashi, and negatively to TSH in Graves. So, more or less, C1q is also associated w/ hypothyroidism.

The symptoms of my Hashimoto occurred at the same time in which my ME symptoms started. So possibly EBV did cause both diseases. I should definitely check for C1q Antibodies...