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I have just listened to the recent Prusty's talk on their unpublished and most recent updates from the lab: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I have just listened to the recent Prusty's talk on their unpublished and most recent updates from the lab: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