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Prusty talks about his upcoming research on a podcast


Listening to this, he has two key ideas
1. the whole thing is caused by herpesvirus reactivation, rather than SARS persistence
2. the symptoms are caused by a "switch" which is the depletion of a key protein.

He says it's something we've never thought of. And it's a protein we can re-introduce, but it will be slow, not an overnight solution.

He didn't give much away, but he does say this:
"the bone marrow is the key because the source of the cells is the bone marrow"
idk, maybe this is about a protein deficiency in platelets, or b-cells, or monocytes?


Senior Member
He also suggests that its EBV reactivation in bone marrow that is the critical piece.

But the missing protein we can reintroduce, that is a big deal. But the treatment is going to be complex and time consuming while all the downstream impacts in the gut and mast cells resolve.
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Moderator Resource
Southern California
A reddit document (not sure if allowed to repost it here) says

This treatment actually already exists for ME/CFS and patients have been successfully treated with it without a scientific explanation

What treatment could he be talking about?
@keepontruckin - it's okay to post the reddit document as long as you post a link where it came from, or you could just post the link - would you do that so we could see it?


Senior Member
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.
The following is a summary of an interview by Bhupesh K Prusty with Sessions TLC (
) in which he explains his theory of the disease Long-Covid and ME/CFS and how they discovered what he believes is an biomarker. He will publish his results soon.

Short takeaway:

The corona virus infects cells and gives Herpesviruses a chance to reactivate, i.e. escape their dormancy. The crucial part is not the corona virus itself, but an event that causes the reactivation of Herpesviruses especially EBV, HHV-6 and HHV-7 and possibly some parvoviruses. This can cause long term mitochondrial dysfunction leading to LC and ME/CFS. This can be reversed/treated by reintroducing a missing protein/biomarker.

Here's a long summary:

Why does not everybody develop LC or ME/CFS? The key lies in the areas where the viruses are reactivated. Two of the key areas seems to be the bone marrow which is a crucial area of the human body as it is the site of B cell development and also neuronal tissues. Furthermore, there are genetic components to how well we fight of a virus once it is reactivated. The body’s mechanism to fight a primary infection can be very different to that of it fighting a reactivated virus.

2 distinct phases of LC and ME/CFS:
  • acute phase of infection (could be lasting up to a year) = Herpesvirus reactivation in specific cells in the tissue (very specific symtoms, often neurological=brain fog or heart related symtoms)
  • chronic phase of disease (includes symptoms such as connective tissue diseases, MCAS, endothelia dysfunction, blood clotting, changes in gut microbiome,…)

The mitochondria plays a crucial role.

In the first phase the mitochondria plays a small role as the herpesvirus is reactivated in very specific regions (neuronal tissue, bone marrow) where the mitochondria doesn’t play a crucial role. The fight is between virus and cells. In this process a certain protein from the herpesviruses is created which creates large scale cell death, inflammation and mitochondria dysfunction in these tissues.

In the chronic phase the mitochondria plays a key role as it is dysfunctional. This leads to cells being in a low energy state which causes the cell danger response and a cascade effect which causes many of the symptoms of the chronic phase. "You take the serum or the isolated factors from an ME/CFS patient, put it in healthy cells, and it causes mitochondrial dysfunction in the healthy cells".

Prusty believes that there is only one theory and one explanation. He does not believe in a replicating SARS-COV-2 virus, but thinks it could be a small possibility. His main argument against it is that LC should then be present more often in people with severe actue Covid. However, it is more common in people with a mild disease.

In his eyes Long-Covid with a duration longer than a year and ME/CFS are very similar.

There are two groups of LC patients:
  • The group that slowly recovers, i.e. the body can drive the reactivated virus back into latency.
  • The group that doesn’t recover whatsoever, they are in the chronic phase of infection for which drugs are needed to escape this.

The biomarker they supposedly found could lead to a treatment. He wouldn't call it a treatment but a switch (analogous to Ron Davis's recent theories). This "biomarker" is present in every human and slowly becomes depleted as the diseases progresses, once this "biomarker" completely depletes to zero one becomes severe. This is what they see, to add a quote from Prusty: "When something goes down (cause), it leads to formation of other unwanted things (effect). That effect can lead to mitochondrial fragmentation". This "biomarker" can be reintroduced into the body as part of a treatment, i.e. this biomarker is very good news. This treatment actually already exists for ME/CFS and patients have been successfully treated with it without a scientific explanation (I am not sure about which treatment he is talking about).

However the treatment will be very complex and time consuming. The switch has to be turned back, i.e. the substance reintroduced and then very slowly secondary diseases (MCAS, SFN, endothelial dysfunction, microclots, ...) could be adressed, this could take years.

He did not reveal the "biomarker", which is a very specific protein, and didn't want to talk about it for very long as he first wants to submit his preprint and then discuss it at the conferences in Berlin & Cambridge (something very sensible!). The key to it lies in the bone marrow and very specific tissue where very specifc cells are created (I would assume B-cells). His earlier papers (for instance https://journals.aai.org/immunohorizons/article/4/4/201/4109) revelead that there is something in the serum of patients that causes mitochondrial dysfunction this biomarker is what causes this dysfunction.

He believes the uncovering out their find will lead to major discussions and a to revolution in the treatment of these diseases.

Overall he came across really well, kind and knowledgeable and much better in this interview than in recent posts on social media. He has explained his reasons we he had pre-announced his work.

Finally, I cannot say that this summary is a perfect summary of the interview as mistakes are possible, if so please point these out. I am a simple layman not an expert like Prusty.

It goes without saying that this is currently just an interview without any published scientific backing, nor has it been verified on a larger set of patients and controls of various conditions. Whether this is Nobel prize winning stuff or not will be seen in the upcoming weeks.

I should also have to mention that these are just some of Prusty's thoughts during a short interview which he rightfully believes is not the right place to explain his full theory. He will do so in his preprint and at the conferences, where he can have an engaging discussion with his peers. This engaging discussion and bringing the work to the light without it going unnoticed is why he made an announcement of his announcement of the biomarker/theory, especially since this is rather a rediscovery of something that has appeared before and he was able to connect the dots.

Rufous McKinney

Senior Member
The Reddit post is a summary of the interview and Dr. Prusty's theory

thanks for posting this super valuable update here. I feel almost OPTIMISTIC something might give.

Its making me CURIOSER and CURIOSER.

What about the Mechanical Theory?

What about correcting the nannoneedle?

Or the Tryptophan model/the Trap?

How might all these varied theories interface into one grand FIX?