Prusty talks about his upcoming research on a podcast

O

Osaca

Senior Member
Messages
344
I'm sure there will be. Video attendance is possible, so someone could make a recording of that.
 
T

Tsukareta

Senior Member
Messages
150
2 weeks away, how do we know he will talk about the CFS research and not something else about viruses in general ? I wonder if the 'protein' is something we can already get a test for without the support of our respective medical industry, as people here probably know the UK gov are not great about CFS, I tried to get diagnosed since late 2020 after at that time having symptoms very specific to CFS for 5 years prior and I was so far unable to be diagnosed with it.
 
S

Sizzle

Messages
93
Tsukareta said:
2 weeks away, how do we know he will talk about the CFS research and not something else about viruses in general ? I wonder if the 'protein' is something we can already get a test for without the support of our respective medical industry, as people here probably know the UK gov are not great about CFS, I tried to get diagnosed since late 2020 after at that time having symptoms very specific to CFS for 5 years prior and I was so far unable to be diagnosed with it.
Click to expand...
He has just 20 minutes. let's not forget this (from the TLC podcast site)
Dr Prusty hopes to publish his findings in the next month, and will present his model at the 12th Invest in ME Research Biomedical Research for ME Colloquium #BRMEC12 and 15th International ME Conference #IIMEC15 2nd June.
 
Murph

Murph

:)
Messages
1,803
O

Oliver3

Senior Member
Messages
936
Tsukareta said:
I already considered that and its definitely a counterpoint to the idea that many CFS cases are caused by unrecognised possibly historic mold exposures, because the symptoms of LC seem to be different enough. Viruses are implicated in some of these mold associated illnesses though, I had new issues in 2020 and 2021 but I didn't start to get the really impactful new symptoms like degraded wrist joints until shortly after I had a bad virus in december of 2021 which gave me a 40c fever and I actually ended up going to hospital over it because I couldn't eat or drink initially which made me think maybe I had pancreatitis, it happened the day after drinking lots of alcohol and having a big campfire in the middle of winter ( my functioning level was relatively good for CFS person at that point ). In the Lake Tahoe incident there was a mystery 'chinese flu' which was blamed for causing the epidemic, then it changed to EBV re-activation because there was a new test which could detect it. The overarching theory is that exposure to some types of mold particularly stachybotrys weakens or disables the immune system which means that when you then have a virus it causes chronic disease, which doesn't seem too far out of line with what Prusty is sort of talking about. This is opposed to people who say that levels of mycotoxins in their body make them ill, or chronic inflammation caused by a sensitivity to the spores ( CIRS ). I can't test if I have CIRS because the very specific tests for it are not really available to the average person in the UK and I can't afford some private doctor.
Click to expand...
I wonder what the precipitating vulnerabilities are. Not everyone exposed to any type of mold suffer issues. So either at the first sight. There's smthg genetic to this.
It's crazy to rule anything out at this point, so I'm not disputing what you're saying .
I just hope prusty has some treatment
 
O

Osaca

Senior Member
Messages
344
I thought it could be interesting to go through Prusty's Twitter profile and there are only two comments relevant for this dicussion that Prusty recently liked:
  • “The thing causing mito fragmentation was for a pwME subset the C1q auto abs. So when you showed that in 2019 I ran to get tested & I was positive. So maybe there’s something missing in the complement system (innate immunity), which is the first line of defence, now malfunctioning”
  • “Does a MBL2 gene mutation and subsequent mannose-binding lectin deficiency establish a vulnerability/predisposition for disease in your model?”
The first one is about the high levels of anti-C1q aabs we’ve already talked about.

The second one is a comment about a MBL2 gene mutation which leads to a deficiency in the protein mannose-binding lectin (MBL). MBL plays an important role in the immune system by fighting foreign invaders by attaching to them. This attachment then activates the lectin complement system. It is an alternative pathway to the classical complement C1q pathway with a similar mechanism. The clinical significance of MBL-Deficiency is debated and it seems like it only leads to a higher susceptibility to infections (unlike C1q deficiency, which leads to Lupus-like diseases). As of today reduced MBL levels seem to play some role in ME/CFS, but the results aren’t really significant, especially when compared to controls https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8465819/ (funnily enough Prusty was the editor of this paper!). It is something that also sees to play a part in Post-Covid Syndrome (https://www.nature.com/articles/s41467-022-32507-6) and is something that for example Scheibenbogen tests for in her current IA trial (https://clinicaltrials.gov/ct2/show/NCT05710770). Both C1q and MBL modulate cytokine production at the mRNA and protein levels and as such play an important role at in the inflammatory response and the avoidance of autoimmunity.

MBL also has a second role, sort of as dirt “cleaner”, in which it binds senescent and apoptotic cells and enhances engulfment of apoptotic cells, as well as cell debris by phagocytes.

MBL is known to bind to SARS-COV-2, HIV, influenza A and seems to play a very small role in HSV-2, HSV-1. The relationship between MBL deficiency and HHV-6 and EBV is not really proven by anything substantial/interesting to us.

Finally there are no treatments at all, or that I could find, that address MBL deficiency. Furthermore it’s mostly produced in the liver and hardly has a connection to the bone marrow.

To summarise: Something to keep an eye on for the future, but probably nothing revolutionary, unless one of you can find out something that I was not able to.
 
Forummember9922

Forummember9922

Senior Member
Messages
189
annaloecher said:
he doesn’t say C1q is high in MECFS patients. he has found high levels of anti-C1q autoantibodies which target C1q. therefore C1q is low in MECFS patients.
Click to expand...
Well this certainly won't make anything clear but heres a non Prusty study that says c1q was high in cfs https://pubmed.ncbi.nlm.nih.gov/34575280/
"Unexpectedly the study also revealed high levels of circulating complement factor C1q in 107/250 (43%) of the participants, placing C1q as a key molecule to identify an ME/CFS subtype/subgroup with more apparent pain symptoms."

It’s a very short 20 minute talk (as are the others)
Click to expand...
That does seem quite brief! One thing that I like about Prusty is that he is relatively well spoken and has personality. I think theres unlocked power of social media and podcasts to gain attention and generate discussion that we need as others have noted. Hopefully we can get more interviews, videos and podcasts from these geniuses like Phair, Davis, Prusty and all the others.
 
Last edited:
failedvulcan

failedvulcan

Messages
7
Is it me, or is there a really worrying lack of emphasis on PEM in Prusty's papers already published? I was looking at a paper published in 2018 and he identifies fatigue as the main feature of ME/CFS, I don't think PEM is even mentioned, yet it is this which distinguishes ME and actually cripples most of us. Of course we are fatigued, but if that was the main symptom we would simply have chronic fatigue, not ME. Many of us could actually safely push through at least some of that fatigue - we know this because people go on far too long pushing through and deteriorate horribly as a result, and even do courses of GET and end up in wheelchairs as a result. But having PEM means we simply cannot safely do that. Is it in fact the case he has come up with something that addresses fatigue but which will make absolutely no difference to us at all because it does not prevent PEM? Frankly a 'treatment' that addresses fatigue is useless to me, it will just add to my intense frustration daily, as I still won't be able to do any more than I can already below my PEM threshold. Please tell me I'm wrong and that he hasn't failed to grasp the nature of ME at all.
 
lyran

lyran

Senior Member
Messages
199
BrightCandle said:
This study might be a clue since they found none existent proteins associated with Long Covid

https://attheu.utah.edu/facultystaff/study-finds-causes-of-long-covid-symptoms/
Cytokines specifically the ones for repair of damage.
Click to expand...

I think this is the actual study.

We compared plasma cytokine levels from individuals with long-COVID to healthy individuals and found that those with long-COVID had 100% reductions in circulating levels of Interferon Gamma (IFNγ) and Interleukin-8 (IL-8). Additionally, we found significant reductions in levels of IL-6, IL-2, IL-17, IL-13, and IL-4 in individuals with long-COVID.
 
Forummember9922

Forummember9922

Senior Member
Messages
189
those with long-COVID had 100% reductions in circulating levels of Interferon Gamma (IFNγ) and Interleukin-8 (IL-8).
Click to expand...
Wow. Ignoring that Prusty may be on to the same thing, and that he may also have some big revealing's of his own, is this statement alone as huge of a deal as it seems? 100%? I wonder what the therapeutic implications might be.

Maybe that paper/article should have it's own thread
 
Last edited:
AnishME

AnishME

Messages
6
I wonder sometime that somebody will be ever able to solve CFS/ME.

It's a different disease for everyone Or atleast different subsets exists but maybe share a common switch for all these symptoms.

Viral reactivation, gut dysbiosis, autoimmune, mitochonidrial dysfunction these are the subtypes I know but what I think all these share a common switch which causes these symptoms
 
S

Sizzle

Messages
93
lyran said:
I think this is the actual study.

We compared plasma cytokine levels from individuals with long-COVID to healthy individuals and found that those with long-COVID had 100% reductions in circulating levels of Interferon Gamma (IFNγ) and Interleukin-8 (IL-8). Additionally, we found significant reductions in levels of IL-6, IL-2, IL-17, IL-13, and IL-4 in individuals with long-COVID.
Click to expand...

For the ones interested, the complete preprint

https://www.medrxiv.org/content/10.1101/2022.10.03.22280661v1.full-text

AI generated conclusion

The paper suggests that individuals with long-COVID have reduced levels of certain cytokines, which are important for healing and fighting off infections. Specifically, they found that those with long-COVID had 100% reductions in circulating levels of interferon gamma (IFNγ) and interleukin-8 (IL-8), as well as significant reductions in levels of other cytokines. The authors propose that immune exhaustion may be the driver of long-COVID, as the absence of these cytokines prevents the lungs and other organs from healing after acute infection and reduces the ability to fight off subsequent infections, contributing to the myriad of symptoms suffered by those with long-COVID.
 
T

Tsukareta

Senior Member
Messages
150
I just doubt that LC thing is what hes discovered, considering the research he was doing probably ran concurrently, and i'm not sure he would describe it as a 'protein' that nobody had thought of before if it was a cytokine, which have been tested before in ME/CFS.
 
You must log in or register to reply here.
Back