Research news from Bhupesh Prusty

SNT Gatchaman said:
In response to question: "Are you saying that you won’t mention the biomarker?"
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"We will announce a biomarker for #MECFS and #LongCovid very soon. A very interesting piece of the puzzle to unfold in coming weeks. Knowingly I did not use the word 'Novel Biomarker' as a lot is known about it and that is actually a very good news. Fingers crossed!" March 23, 2023

 
I can see why he wants to describe it properly. It could be important, and if it turns out he's made a fundamental discovery, he deserves to get the credit.

But why not just wait for the conference? He could have used it to give the heads-up that he may have found a link between ME and PASC and possibly even a biomarker for PASC and severe ME, with a 'watch this space' for the preprint. It would have been much more credible way to make the announcement, and there would have been a significant ripple of anticipation.
 
Great news. Bhupesh Prusty et al's research article can be read here:
https://journals.aai.org/immunohori...uman-Herpesvirus-6-Reactivation-Mitochondrial


Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multifactorial disorder with many possible triggers. Human herpesvirus (HHV)–6 and HHV-7 are two infectious triggers for which evidence has been growing. To understand possible causative role of HHV-6 in ME/CFS, metabolic and antiviral phenotypes of U2-OS cells were studied with and without chromosomally integrated HHV-6 and with or without virus reactivation using the histone deacetylase inhibitor trichostatin-A. Proteomic analysis was conducted by pulsed stable isotope labeling by amino acids in cell culture analysis. Antiviral properties that were induced by HHV-6 transactivation were studied in virus-naive A549 cells challenged by infection with influenza-A (H1N1) or HSV-1. Mitochondria were fragmented and 1-carbon metabolism, dUTPase, and thymidylate synthase were strongly induced by HHV-6 reactivation, whereas superoxide dismutase 2 and proteins required for mitochondrial oxidation of fatty acid, amino acid, and glucose metabolism, including pyruvate dehydrogenase, were strongly inhibited. Adoptive transfer of U2-OS cell supernatants after reactivation of HHV-6A led to an antiviral state in A549 cells that prevented superinfection with influenza-A and HSV-1. Adoptive transfer of serum from 10 patients with ME/CFS produced a similar fragmentation of mitochondria and the associated antiviral state in the A549 cell assay. In conclusion, HHV-6 reactivation in ME/CFS patients activates a multisystem, proinflammatory, cell danger response that protects against certain RNA and DNA virus infections but comes at the cost of mitochondrial fragmentation and severely compromised energy metabolism.
 
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multifactorial disorder with many possible triggers.

I really wish people would not say this. The simple truth is that we just don't know enough about it all to allow such definitive statements.
 
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Prusty doesn’t seem hugely concerned about consistency of narrative, and he may not always consider the potential impact of tweets before he presses send.

But. Thursday is obvious an incredibly important day in the ME calendar and a force multiplier on any academic findings publicised that day. We should be able to forgive someone who is going to make some sort of contribution to biophysical ME research - even if only by closing off a blind alley - for trying to make the timings work to his advantage, and for seeking all the attention he can get, if it helps him secure funding.

In the meantime, caveat lector.
 
Shadrach Loom said:
Yes, but also with a strong sense that the onus is on the reader to do their due diligence. The original phrase “caveat emptor” (let the buyer beware) is used by lawyers and others wanting to establish formal limits on the obligations of vendors.
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I don't think that legions of sick and house or bedbound people should have to 'beware' when they read tweets from someone who is supposed to be a legitimate researcher.

If Prusty has uncovered anything less than a smoking gun he has acted with callous disregard for patients.
 
V.R.T. said:
I don't think that legions of sick and house or bedbound people should have to 'beware' when they read tweets from someone who is supposed to be a legitimate researcher.

If Prusty has uncovered anything less than a smoking gun he has acted with callous disregard for patients.
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This is just a tremendously weird field, through no fault of our own. But funding for proper research is very scarce whilst anyone that says they want to talk patients out of their disease seems to be getting awarded money right, left and center. Whilst I do not enjoy being jostled in the way Prusty has done I can sort of get why he does it. @Shadrach Loom alluded to it, you need to build a fair bit of hype if you want to obtain funding. OMF has been doing just that. They've got Nobel laureates on their board who's most important function seems to be to create hype just by their standing. And it seems to have worked some for them.

The situation being as it is, I can understand the need for researchers to advertise themselves and their work if they ever want any funding. It's a rotten situation to be in and I can't say I enjoy being hyped up and subsequently let down. As long as he's legitimately interested in helping us forward I can deal with it though.
 
Solstice said:
you need to build a fair bit of hype if you want to obtain funding. OMF has been doing just that. They've got Nobel laureates on their board who's most important function seems to be to create hype just by their standing. And it seems to have worked some for them.
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And sometimes making things appear bigger than they really are attracts funding. Who knows where it will go, but it's better than doing nothing?

I no longer get hyped but I appreciate Prusty's passion.
 
Even if what will finally get presented in June is more modest than expected, it won't leave us with nothing I think. While I have not read all of his stuff, I've read enough (like e.g. How herpesviruses awaken) to see that he's looking at something very cool and relevant, which connects to earlier observations, and that he's part of a growing understanding of WTF is happening in our bodies.

Even if it's not a biomarker, there will be markers and more understanding of very key mechanisms. At this moment I can forgive him his "sneak previews without the actual previews", it might not be great to do, but it seems he's bursting to share it. I like a researcher with such passion.

If he would turn out to be a bag of hot air (which I doubt), he'd lose the trust and goodwill of an important part of the patient community - I doubt he's that stupid.
 
Well, I've just watched Prusty's talk at the Berlin conference and I'm none the wiser. It was the end of a long day, much of the detail was too complicated for me, and he kept moving away from the microphone so I missed bits.

He did at the end talk about some things they've found that correlate with disease severity. Something to do with circulating immune complexes in ME/CFS and high and low levels of some things labelled as TF, A2M and FNI which I think he said was fibronectin which was high in serum but low in ???

I hope someone with more understanding of his work can enlighten us.
 
I made a note of the astronauts reference. It wasn't part of his talk but the previous speaker mentioned in passing that reactivation of EBV is found in astronauts that normalises once they are back on earth. Prusty, before starting his talk, responded to that by saying that returning astonauts had mitochondrial fragmentation.
 
Can elevated amount of circulating fibronectin be the Something in the Blood that Davis was looking for? The signaling protein?

“Fibronectin (FBN) is an extracellular matrix (ECM) component that, through binding integrin receptors of the cell surface, acts as a key player of the communication between the intra and the extracellular environment, thus controlling cell behavior.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928270/
 
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The chart on the differences in fibronectin in serum between healthy controls and ME/CFS was a bit underwhelming - there's an awful lot of overlap. As Trish says, it was all pretty rushed, so hard to know for sure. Perhaps it's part of the problem, at least for some people, or perhaps it's a downstream consequence of the illness. Whatever, it doesn't work as a biomarker, at least not on its own.
 
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