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 how they discovered what he believes is an biomarker
. He will publish his results soon.
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.
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.