Research news from Bhupesh Prusty

To me he comes across as a person who genuinely emphasises with pwME. I don't think he ever intends to give false hope,
thats fine, but intent doesnt change the end result, if you trap someone hand in a car door by accident, the fact that it was an accident doesnt stop the persons fingers being crushed.

He comes across as very genuine and kind.
I'm sure he is, & i am very grateful for his efforts. I just wish he'd allow that kindness to extend to 'best not give teasers until i'm ready to explain it all, because leaving despertae people hanging for months, is cruel'. And 'I'd better not hype it up to be a biomarker unless i'm absolutely certain beyond all doubt, because raising hopes that turn out not to be fulfilled is a form of torture for people who are suffering'.

I'm not saying he is thinking this - i obviously dont know what he's thinking but i can imagine the intense desire to help people you care about, coupled with excitment about your own discoveries, can loead to thinking things such as 'i'll give them a little snippet just to encourage them, to let them know that there is hope & that there's some big news coming'.

Its a very human thing to do when you care, & it might seem kind & caring & encouraging...... but it just reveals that they have no idea what its like to have been on the receiving end of such things... for decades, ovber & over & over again, with none of it ever coming to fruition or turning out to be real. No actual answers.

Dashed hopes is one of the cruellest, most distressing things when it happens repeatedly over years, it messes with your head & your heart.

I just wish they would all stop doing it. As i said before - teaser posts are utterly inappropriate in the context. And if English isnt your first language, then be careful & get someone whos 1st language is english, to check it first. Just please, have a care for the msg you're sending

Edit: i may be not being very gracious/patient, i'm sure he's doing his best, but i am at the end of my rope.
 
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"Today we also restarted our quest to scan almost the entire human body for localizing potential sites for viral infection, which might be a source of trigger for ME/CFS. In coming months we will test biopsies from most of the human body parts including the entire brain".

This is what I was concerned about, possibly making connections with viral infections and the hypercoagulation state theory.


This is what David Berg was going on about 23 years ago. From one of his Townhalls:

[David] I trust that the combined information from last week and this week
makes sense and is logical. The coag Paradigm Shift is that we should now
treat patients with fibrin deposition as we treat patients who have had a
blood clot. The new protocol on our web site (www.hemex.com) [which will be
modified tomorrow], should help most CFIDS patients get back to almost
complete health for under $3000, including lab testing, TF(transfer factor), antibiotics and
physician charges. There will always be the coag protein defect in the
patients, but once the infection is treated completely, then the protein
defect can be monitored over time. When a relapse occurs, use heparin to
control the infection quickly before becoming a CFIDS patients again.
Remember, the longer one has been ill, the longer it may take to get rid of
the HHV6.

I can't believe this made sense to me over 20 years ago. Taking TF and Imunovir changed the course of my illness and made me worse, permanently.
 
This had better actually be something otherwise it's absolutely abhorrent to play with people's hopes this way. People like me can't cope with the rollercoaster of self promotion and let down. we need honesty not marketing
 
"We will announce a biomarker for #MECFS and #LongCovid very soon. A very interesting piece of the puzzle to unfold in coming weeks".

A biomarker for both.

Prof Akiko Iwasaki in the above tweet says: "Low cortisol levels were the strongest predictors for both defining Long Covid status and disease severity".

This has not been shown to be the case in pwME.
 
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Given his prior work and the fact that he specifically referenced "our paper from 2020" (presumably this one), that would cover point #4.

That abstract concluded —

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.

Some body quotes from that paper —

These results suggested that an unknown and IFN-independent transferrable factor from HHV-6A–reactivated cells can induce a hypometabolic, fragmented mitochondrial phenotype in responder cells.

A plausible explanation can be localized viral infection/activation in distant parts of the body, thereby releasing a few infected cells carrying activated virus or releasing some of the activation-mediated cellular factors into the blood stream.

miRNAs regulate intra-organellar mechanisms, in which they perform the job of fine-tuning of the functions required to fulfil the metabolic demands of an organ or cell type. Our previous deep sequencing approach revealed major changes in the expression of a large panel of human miRNAs upon HHV-6A reactivation that hints to a broad range of effects on mitochondria and associated metabolic functions upon viral activation.

we show that incomplete HHV-6 reactivation, even in a small fraction of latently infected cells, causes reactivated cells to secrete an activity that can be transferred in serum and produces mitochondrial fragmentation and coordinates a powerful antiviral program in responding cells.

Unlikely to have included #2 in this new work but possible. I think cortisol (#7) is irrelevant or a red herring.

If it's borne out that this is a valid biomarker for mito fission (?? specific miRNA ± supported by dUTPase/Abs ± some other immune/metabolic features as above), then by extension I guess point #1 would be inherently replicated also.

---
Key references in the above body quotes are —
HHV-6 encoded small non-coding RNAs define an intermediate and early stage in viral reactivation (2018)
Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome (2016)
 
I... asked if his biomarker collaborates any of her findings...

I think you mean corroborates, not collaborates.
Verb: confirm or give support to (a statement, theory, or finding).
3rd person present: corroborates; past tense: corroborated; past participle: corroborated; gerund or present participle: corroborating
"the witness had corroborated the boy's account of the attack"
 
I think you mean corroborates, not collaborates.
Verb: confirm or give support to (a statement, theory, or finding).
3rd person present: corroborates; past tense: corroborated; past participle: corroborated; gerund or present participle: corroborating
"the witness had corroborated the boy's account of the attack"
Either variation of the word works, at least over here in the US. I'm just glad to see 2 major (but independent) researchers see something similar. Now I'm starting to think of Dr Chia and his EBV claims.
 
Is it me, or are parts of that list from Prof Iwasaki a bit underwhelming?

Would it be very surprising if 94% of patients who said they were ill turned out to be ill, or if immunisation increased antibody responses, or if herpesviruses reactivated during illness, or if no increased autoantibodies were observed, or if low cortisol produced symptoms or exacerbated existing ones?

It might be that there are specific meanings in there that I, as a non-medic, haven't understood. I hope so, because it would be great if they had found something new and interesting.
 
Is it me, or are parts of that list from Prof Iwasaki a bit underwhelming?
I had the same thought. The 94% one is particularly odd.

"Patient Reported Outcomes alone are sufficient to identify long COVID patients with 94% accuracy."

That assumes that there is a method to identify long COVID patients that has 100% accuracy. Else, how you could you possibly know how accurate the Patient Reported Outcomes are? Stuff like that erodes confidence pretty quickly.
 
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