Prusty talks about his upcoming research on a podcast

godlovesatrier

godlovesatrier

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@Treeman hope not as none of us have a hope of getting it - did you get it by the way in the end?

He also said that in LC/covid infection the covid infects the cell and then the hhv-6 comes along nad takes over the infection in the cell pushing the covid out of the cell - meaning he said that the hhv-6 is the issue, not the covid rna. But later he did say that he can't be 100% sure about this, but it's what he's seen in his research. I thought that was very interesting.

I also thought the podcast shed a lot of light on why people did better for remission on valcyte than they did valtrex.
 
Mary

Mary

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Rufous McKinney said:
even if It may not come thru, for me (having been sick for decades upon decades and now I have lymphoma (found out today)
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@Rufous McKinney - when it rains (and we all know how much rain California has had this year!) . . . . it ain't fair! Okay, we are all rooting for you and sending good thoughts/positive energy etc. your way - take care and keep us posted - :hug:
 
Treeman

Treeman

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MonkeyMan said:
What drug are you referring to, please?
Thank you.
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Hi, as well as a ME/CFS diagnoses I have hypogammaglobulinamie. My daughter has also now been diagnosed with the same Illnesses and we both commenced 2 months ago immunoglobulin therapy.

We are also undergoing genetic testing as they believe our illness is a primary immune disease.

My daughter has been ill around a couple of years and is showing great signs of recovery, including reduction of fatigue.

My situation is I think I'm showing only slight signs of recovery but I've been ill for over 50 years.

I can see similarities with what Prusty says, the longer you've been ill, the longer to recover.

Additionally he also says the treatment is already been used, could he be referring to immunoglobulin therapy?

People treated with immunoglobulin therapy all suffer from debilitating fatigue and the vast majority see that fatigue reducing with treatment.
 
Forummember9922

Forummember9922

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Vlad83 said:
Based on some clues from his interview and this video I chatted with GPT4 and got some candidates:



#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.
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Pretty cool stuff. I think watching that lecture video really shows how important this fragmentation issue is, and the ring that gets a chokehold on the mitochondria- I really enjoy hearing Prustys explanations.

Which of these on the list could also be in line with his hint of
‘when this protein is gone another thing goes up causing issues’? Mdivi1 gone so drp goes up?

I feel silly pretending like I understand this and I just pray Prusty will continue to be a soldier in this high stakes war.
 
V

Vlad83

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Forummember9922 said:
Which of these on the list could also be in line with his hint of
‘when this protein is gone another thing goes up causing issues’? Mdivi1 gone so drp goes up?
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No idea.

I really don't know what I am talking about, but ChatGPT seems to :)

I basically just asked it to list all related proteins and then all the drugs that target any of them. Then googled each one, and lo and behold, IV cyclosporine shows up here: https://meassociation.org.uk/2021/0...ging-treatment-options-for-autoimmune-me-cfs/ It also shows up in one of Nancy Klimas papers as a potential target.

Prusty did say that a drug that is already available is being trialed, and he also alluded on Twitter that a supplement won't do it, which rules out some possibilities. Then Phair says here that there's nothing wrong with mitochondrial membranes, and it's just fission that is being targeted, so that rules out some more.

So my bet is on cyclosporine :)
 
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V

Vlad83

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Some more possibilities:

List any drugs that affect molecular pathways related to mitochondrial fission, fusion or quality control.

Mitochondrial dynamics and quality control are essential processes for maintaining cellular homeostasis and proper mitochondrial function. Several drugs and compounds have been identified that modulate these processes by targeting the molecular pathways involved in mitochondrial fission, fusion, or quality control. Some of these drugs include:
  1. Mdivi-1 (Mitochondrial Division Inhibitor-1): Mdivi-1 is a selective inhibitor of the mitochondrial fission protein, Drp1 (dynamin-related protein 1). By inhibiting Drp1, Mdivi-1 reduces mitochondrial fission and promotes mitochondrial elongation.
  2. Leflunomide: This immunomodulatory drug is known to inhibit mitochondrial fusion by targeting the Mfn1 (mitofusin 1) and Mfn2 (mitofusin 2) proteins.
  3. Metformin: Metformin, a widely prescribed antidiabetic drug, has been shown to affect mitochondrial dynamics by promoting fusion and inhibiting fission, potentially through the activation of AMP-activated protein kinase (AMPK) pathway.
  4. P110: P110 is a peptide that promotes mitochondrial fusion by targeting the OPA1 (optic atrophy 1) protein, which is involved in the regulation of mitochondrial inner membrane fusion.
  5. SS-31 (Elamipretide): A mitochondria-targeting peptide that has been shown to improve mitochondrial function and reduce oxidative stress, it is thought to act by stabilizing cardiolipin, an essential phospholipid in the inner mitochondrial membrane.
  6. Spermidine: Spermidine is a natural polyamine that has been shown to induce mitophagy, the selective degradation of damaged mitochondria by autophagy, thereby promoting mitochondrial quality control.
  7. Rapamycin: This immunosuppressive drug has been shown to induce mitophagy and promote mitochondrial quality control through the activation of the mTOR (mammalian target of rapamycin) pathway.
  8. NAD+ precursors (e.g., Nicotinamide Riboside, Nicotinamide Mononucleotide): These compounds can boost cellular NAD+ levels, which in turn can promote mitochondrial quality control by enhancing the activity of sirtuins, a family of NAD+-dependent protein deacetylases that regulate various cellular processes, including mitochondrial biogenesis and dynamics.

We are looking for drugs that promote fusion and inhibit fission, so that points to:
  1. Mdivi-1
  2. Metformin
  3. P110
 
Rufous McKinney

Rufous McKinney

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Vlad83 said:
So my bet is on cyclosporine :)
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reading about that:

https://medlineplus.gov/druginfo/meds/a684054.html
"Receiving cyclosporine injection may increase the risk that you will develop an infection or cancer, especially lymphoma (cancer of a part of the immune system) or skin cancer."

Which merry go round is this? I am to take something that might improve the ME only it might give me the lymphoma I am told I already have?
 
BrightCandle

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I really don't know what he is hinting at. Looking at the 2020 paper (https://pubmed.ncbi.nlm.nih.gov/32327453/) its not obvious which of the identified proteins are the likely issue that they found and then later understood. Supplement A (https://journals.aai.org/immunohori...4109/pdf/ih_2000006_supplemental_materials_1/) contains a list of the protein changes after cell infection with purple being significant which leads to a list of:

CYP4F2;CYP4F3
DHRS2
TYMS
DUT
UBE2C

But then in the paper also called out are downregulatrion of PDP1 and SOD2 and altered pyruvate dehydrogenase.

retinoic acid is mentioned as part of the innate response for mitochondira fragmentation too.

Whatever this protein is it needs to cause fusion of the mitochondria since this seems to be the entire point of Prusty's work at this point showing HHV6 fissions the mitochondria and results in reduced innate immune response to the reactivated virus and the body must run out of this thing and then fail to fuse enough mitochondria to kick the virus back into latent state. The paper also says that a single infected cell will impact its neighbours too.

None of the proteins ChatGPT think cause fission (DRP1, MFF, MiD49, MiD51, and FIS1,) appear in the paper as a substantial change or marker in the work where he is testing if ME/CFS cells show similar patterns when removed from patients later in the paper. So I genuinely have no clues from going through this paper all these years later!

PS I sort of love how Chat GPT has become a helper in this type of research, its a useful tool although it may be confidently lying to us!
 
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