Prusty talks about his upcoming research on a podcast

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Vlad83

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I believe this is the first presentation (May 11 or 12).
 

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Oliver3

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Vlad83 said:
I believe this is the first presentation (May 11 or 12).
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What I would like to know is, why isn't the condition passed from person to person via contact. If you have reactivated heroes why does somobe else's immune system work better.
If they're dropping serum into normal blood and it's creating issues , why doesn't this happen to loved ones during intimacy
 
Judee

Judee

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junkcrap50 said:
The Reddit post is a summary of the interview and Dr. Prusty's theory. I quoted it below to save people a click. Make sure to click expand to read the whole thing.
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Thank you!!!

Thank you for doing all that @junkcrap50.

I do watch yt videos but something more in depth like this I do better reading (and re-reading) it try to absorb. There may be others here as well like me who you are helping tremendously.
 
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Oliver3

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Vlad83 said:
I think he said the defective cell-autonomous response to HHVx could be genetic. Whether this leads to disease is random (depends on the tissue where the reactivation occurred)
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Could defective thing be a subset of collagen expression?
 
wabi-sabi

wabi-sabi

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Oliver3 said:
possible to contract through sex..so why not this.
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As I understand, with ME/CFS it's not the virus, but the body's response to the virus, especially the innate immune system. With HIV etc, it's the virus itself that is being passed as well as causing the problem. 90% of adults have EBV, but only some of those get ME/CFS from it.
 
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Oliver3

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That makes sense but the million dollar question is why I guess still isn't it...guess we have to wait....thanks for that
 
Forummember9922

Forummember9922

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FWIW here is a previous lecture he gave a few years ago, not sure how his views may have changed since this time
'Pathogenic alterations of mitochondrial dynamics: A working model of ME/CFS'

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Vlad83

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Based on some clues from his interview and this video I chatted with GPT4 and got some candidates:

List all proteins that are in any way related to Drp1 or interact with it or are in the same pathway

Drp1 (dynamin-related protein 1) interacts with various proteins and is part of a complex network of pathways related to mitochondrial dynamics, including fission, fusion, and quality control. Here is a non-exhaustive list of proteins that are related to Drp1 or interact with it, or are in the same pathway:
  1. Fis1 (Mitochondrial fission 1 protein): A protein on the outer mitochondrial membrane that helps recruit Drp1 to the mitochondria during fission.
  2. Mff (Mitochondrial fission factor): Another protein on the outer mitochondrial membrane involved in Drp1 recruitment for mitochondrial fission.
  3. MiD49 (Mitochondrial dynamics protein 49): Involved in Drp1 recruitment and regulation of mitochondrial fission.
  4. MiD51 (Mitochondrial dynamics protein 51): Similar to MiD49, involved in Drp1 recruitment and regulation of mitochondrial fission.
  5. OPA1 (Optic atrophy 1): A protein involved in mitochondrial fusion, mainly responsible for the fusion of the inner mitochondrial membrane.
  6. MFN1 (Mitofusin 1) and MFN2 (Mitofusin 2): Proteins responsible for the fusion of the outer mitochondrial membrane, counterbalancing the fission process driven by Drp1.
  7. PINK1 (PTEN-induced kinase 1): A kinase involved in mitochondrial quality control, which phosphorylates several proteins, including Drp1, to regulate fission and mitophagy.
  8. Parkin: An E3 ubiquitin ligase that works together with PINK1 in mitochondrial quality control and mitophagy.
  9. SUMO (Small ubiquitin-like modifier): A family of proteins that can post-translationally modify Drp1, affecting its function and regulation.
  10. Calcineurin: A protein phosphatase that can dephosphorylate Drp1, modulating its activity in response to changes in cellular calcium levels.
There are many other proteins that could interact with or regulate Drp1 in various cellular contexts, and the list above is not exhaustive. The understanding of the relationships and interactions between these proteins is constantly evolving, and more research is needed to fully elucidate the complex network of pathways involving Drp1.

List all commercially available drugs that are in any way related to any of these proteins

Several commercially available drugs have been found to affect or interact with the proteins mentioned in the previous response, which are involved in mitochondrial dynamics and function. The following is a non-exhaustive list of such drugs:
  1. Cyclosporine A: An immunosuppressive drug that inhibits calcineurin, affecting its ability to dephosphorylate Drp1 and modulate mitochondrial dynamics. It is used to prevent organ transplant rejection and to treat certain autoimmune diseases.
  2. FK506 (Tacrolimus): Another immunosuppressive drug that inhibits calcineurin, similar to Cyclosporine A. It is used for organ transplant rejection prevention and in the treatment of certain autoimmune diseases.
  3. Mdivi-1 (Mitochondrial division inhibitor 1): A small molecule inhibitor of Drp1, which has been investigated for its potential neuroprotective effects. Although it is not yet an approved drug for any specific condition, it is commercially available for research purposes.
  4. NIM811: A non-immunosuppressive cyclosporine A analog that has been shown to inhibit mitochondrial permeability transition and protect against ischemia-reperfusion injury. It is currently in the experimental stage and is not approved for clinical use.
  5. S1R agonists (e.g., pridopidine): Sigma-1 receptor (S1R) agonists have been shown to modulate Drp1-dependent mitochondrial fission. Pridopidine, an S1R agonist, is under investigation for potential use in treating neurodegenerative diseases like Huntington's disease and Parkinson's disease.
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#1 and 2 have been tried in ME/CFS apparently with some success.

#3, 4, 5 are investigational drugs. I have not found any mention of them being tried for ME/CFS, however Prusty has mentioned Mdivi-1 on Twitter at some point.
 
BrightCandle

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One thing I am considering is that the moment he announces this protein at conference whatever direct drug helps this the most is going to sell out world wide, for months probably years we have all seen the impact of Long Covid purchases on Amazon and such this is going to be just as impactful as the blood clotting finding.

As far as I can tell the two conferences this will be talked in are both in person and paid for although I presume its going to hit social media fairly fast. This is going to be crazy, if it works more so.
 
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