Research news from Bhupesh Prusty

Facebook post from @Simon M

Code:
https://www.facebook.com/topmecfsresearch/posts/907217086399909


Do we know the results of a healthy cell in control serum incubated for 24 hours? Is it still different to the healthy cell incubated with 'extract of patient'?

Good question. I had assumed that was part of the study. On Twitter VP said he was using several different controls, so I assumed it would include the obvious.
 
Prusty tweets about a 'cellular component'.

Davis has talked about 'something in the blood', and how filtration puts it at around the size of an exosome.

So, could an exosome (or other extracellular vesicle) be that cellular component? According to Wikipedia, they are a membrane enclosed vesicle secreted by most cells, which can merge with other cells. They can contain proteins, lipids, DNA, RNA and miRNA. Reactivated HHV-6 could go to town and put anything it likes in there. What if it's purpose was to suppress nearby immune cells so that it can spread? (Hanson has recently demonstrated impaired glycolysis in T4 and T8 cells IIRC).

Right now we're seeing a pandemic caused by coronavirus 2019-nCoV which IIRC hijacks the endomembrane system to secrete copies of itself. So we know that viruses really can mess around at this level.

Following through this line of thought. If it were an exosome, and if it had unique surface proteins. Well then one line of therapy might be a vaccine.
 
The thing that gets me hopeful about Prusty's work is that tie up with the 'something in the blood' discoveries that others had made. Although it's not direct validation they're finding things that seemingly tie up. I hope there's a collaboration in the offing. I know that Prusty has tweeted about discussing things with Naviaux.

All the detail is lost on me though!
 
*a 6 minute video on mitochondrial fission & fusion.

The narrator's accent makes it a little difficult to follow (especially if brain fog is bad)



*Mentions signal to fuse or break up comes from cell nucleus but narrator says the reasons is unknown (at time of making in December 2012)

*PS thanks @Simon M for your rather good Facebook explaner
 
*Another 12 minute video which covers mitochondrial fission & fusion comes from the Physionic podacst.



*The author is a PhD student whose research covers mitochondria. This broadcast is more recent. (2019)

*He looks at fission & fusion in terms of mitochondrial DNA. Fusion being a way of removing DNA mutations by being absorbed into another cell.

*The fission happens after fusion whereby the non defective parts of the mitochondrion which do not have mutant DNA are pinched off.

*The mutant DNA being retained for destruction.

*No diagrams but an easier video to follow. The first part is an introduction to mitochondria, the latter part covers fission & fusion.
 
Some more background info on mitochondrial fission via an article from Science. You can get a copy via Sci Hub by inputting the DOI

10.1126/science.1219855

Mitochondrial Fission, Fusion, and Stress
  1. Richard J. Youle1,*,
  2. Alexander M. van der Bliek2,*
  1. *To whom correspondence should be addressed. E-mail: youler@ninds.nih.gov (R.J.Y.); avan@mednet.ucla.edu (A.M.v.d.B.)
Science 31 Aug 2012:
Vol. 337, Issue 6098, pp. 1062-1065
DOI: 10.1126/science.1219855

Abstract

Mitochondrial fission and fusion play critical roles in maintaining functional mitochondria when cells
experience metabolic or environmental stresses.

Fusion helps mitigate stress by mixing the contents
of partially damaged mitochondria as a form of complementation.

Fission is needed to create newm but it also contributes to quality control by enabling the removal of damaged mitochondria and can facilitate apoptosis during high levels of cellular stress.

Disruptions in these processes affect normal development, and they have been implicated in neurodegenerative diseases, such as Parkinson’s.
 
Is there any evidence for this claim of HHV-6 reactivation in MECFS? I thought Ron Davis’ group found no unusual viruses and no high virus levels. Is this HHV6A or HHV6B?
I'm pretty sure he's answered questions like that in his tweets but you'd have to dive into his timeline to find them. I think he's sais something along the lines of the viral infection can be localised, so not necessarily showing up in blood tests. Best find his quotes though as I could be talking rubbish.

ETA: Hopefully we won't have to wait too long for the paper to be published and it'll answer all these types of questions.
 
Is there any evidence for this claim of HHV-6 reactivation in MECFS? I thought Ron Davis’ group found no unusual viruses and no high virus levels. Is this HHV6A or HHV6B?
He has a published paper that shows that when HHV6 infects cells a small non-coding RNA (sncRNA-U14?) can be detected.

He has presented (NIH conference?) that the same small non-coding RNA can also be detected in a large subset of ME patients, but not many healthy controls. So while this does not definitely mean there is HHV6 reactivation, it does hint at the possibility.





And this tweet mentioned that HHV6A was detected in the Lake Tahoe outbreak
 
Is there any evidence for this claim of HHV-6 reactivation in MECFS? I thought Ron Davis’ group found no unusual viruses and no high virus levels. Is this HHV6A or HHV6B?
Clinical evidence. It’s one of the criteria my doc used to diagnose MECFS.
 


"Trying to conceptualize an RNA-based therapy." RNA-based therapy includes RNAi, and antisense therapy which are both used to silence specific mRNAs. I'm wondering if this suggests that the "something in the blood" is an mRNA or a group of mRNAs specific to HHV-6 or other viruses. Or perhaps silencing a specific HHV-6 mRNA makes it so that the virus can't secrete the "something in the blood."
 
I was going to start a new thread but I'll post here instead as my comments concern Bhupesh's tweets. Though I am happy for this to become a new thread.

Dr. Prusty is clearly exploring engaging with patients over Twitter but some of his tweets have left me confused.

First, I'm not sure what is meant by this, at all...


Surely the answer is simply 'publication'. He must know the patient community wait with baited breath for each new publication, and they are widely read. I'm not sure what is implied in the second half of the tweet.


Second, I'm not sure patients sliding into his DM's is the best way of aquiring data.


There are responses suggesting he join some private FB groups. Again, I feel this is not the way forward. Is Dr. Prusty a member here?
 
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