Prusty talks about his upcoming research on a podcast

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Tsukareta

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EBV could be re-activated because the immune system is weakened though, by environmental factors or some other disease mechanism internal to the body, thats the trouble, but also why I think Prustys new thing will be interesting because its more specific.
 
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Osaca

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Tsukareta said:
EBV could be re-activated because the immune system is weakened though, by environmental factors or some other disease mechanism internal to the body, thats the trouble, but also why I think Prustys new thing will be interesting because its more specific.
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We should not forget that this should just be the first of Tim Henrich's pupblications on EBV with many to follow. He's currently been publishing a paper almost weekly on LC (https://scholar.google.com/citations?hl=en&user=g8g2SFAAAAAJ&view_op=list_works&sortby=pubdate) and he sounded ambitious in his interview with Amy Proal. I would expect more answers on EBV once he releases data from his tissue samples, of course the absense of monoclonal ab's for EBV for PET-tagging remains.
 
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Tsukareta

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It would be very interesting to see if theres any overlap between what Prusty says hes going to publish about and the mouse experiment from Simmaron Research, which seems like it could conceivably provide a complete model for the mechanism that causes the symptoms of the disease ( but so far not how that state is setup and sustained ).
 
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Osaca

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Bhupesh Prusty has received 25 000€ of funding for a small study by the Deutsche Gesellschaft für ME/CFS that can now start https://www.mecfs.de/forschungsfoerderung-2022/ .

"The study investigates the link between viral infections (especially HHV-6, HHV-7 and EBV), autoimmunity and mitochondria in the development and progression of ME/CFS. The researchers are using a novel method called Targeted Immunoglobulin Associated Proteomics (TIgAP) to identify proteins that may be targets for ME/CFS-specific antibodies.

The main objective of this study is to apply the immunoglobulin fractions from ME/CFS patients and healthy controls (n = 10 each) to different primary cell types and isolate proteins that specifically interact with the IgG fractions from ME/CFS patients. Subsequently, these proteins will be identified by mass spectrometry and their interactions with IgG will be validated in further studies."

Seems very connected to his announcement. The mention of ME/CFS-specific antibodies is particularly interesting. Have we heard of any proteins that could be targeted by ME/CFS-specific antibodies and what would these antibodies be (GPCR-AAB's don't seem specific enough nor relevant, possibly IgG3 or IgG4, VCA-IgG)? Seem like IgG fractions destroy this protein he's talked about. IgG goes up, protein goes down. IgG is created in B-cells and bone marrow!

It’s also in line with this study https://pubmed.ncbi.nlm.nih.gov/33794313/ that showed that several immunoglobulin genes are significantly increased in ME/CFS patients compared with controls. Furthermore there’s a strong connection to interferon.
 
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junkcrap50

junkcrap50

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Tsukareta

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Osaca said:
Bhupesh Prusty has received 25 000€ of funding for a small study by the Deutsche Gesellschaft für ME/CFS that can now start https://www.mecfs.de/forschungsfoerderung-2022/ .

"The study investigates the link between viral infections (especially HHV-6, HHV-7 and EBV), autoimmunity and mitochondria in the development and progression of ME/CFS. The researchers are using a novel method called Targeted Immunoglobulin Associated Proteomics (TIgAP) to identify proteins that may be targets for ME/CFS-specific antibodies.

The main objective of this study is to apply the immunoglobulin fractions from ME/CFS patients and healthy controls (n = 10 each) to different primary cell types and isolate proteins that specifically interact with the IgG fractions from ME/CFS patients. Subsequently, these proteins will be identified by mass spectrometry and their interactions with IgG will be validated in further studies."

Seems very connected to his announcement. The mention of ME/CFS-specific antibodies is particularly interesting. Have we heard of any proteins that could be targeted by ME/CFS-specific antibodies and what would these antibodies be (GPCR-AAB's don't seem specific enough nor relevant, possibly IgG3 or IgG4, VCA-IgG)? Seem like IgG fractions destroy this protein he's talked about. IgG goes up, protein goes down. IgG is created in B-cells and bone marrow!

It’s also in line with this study https://pubmed.ncbi.nlm.nih.gov/33794313/ that showed that several immunoglobulin genes are significantly increased in ME/CFS patients compared with controls. Furthermore there’s a strong connection to interferon.
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that seems very likely, an autoantibody causing a cascade of effects was always one of the simplest explanations for the disease.
 
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Osaca

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Tsukareta said:
that seems very likely, an autoantibody causing a cascade of effects was always one of the simplest explanations for the disease.
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It also explains the antiviral property of the serum of ME/CFS pateints that Prusty witnessed, which hasn't been explained yet (nor reproduced?).
 
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Osaca

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Rufous McKinney said:
The paper dropped:

https://journals.aai.org/immunohori...uman-Herpesvirus-6-Reactivation-Mitochondrial

Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome​

Immunohorizons (2020) 4 (4): 201–215.

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.
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This is just his old 2020 paper we've been talking about the whole time. But we should get lucky next week ;)
 
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wastwater

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I think the switch maybe in the liver
The viral lowering of complement C3 in the liver leading to uncleaved C5 (high)for immune activation and membrane attack including mitochondria
I wondered if it could be treated like aHUS
 
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Sizzle

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Screenshot_20230507-231945.png
 
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perrier

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Sizzle said:
Don't know, but doesn't sound like a treatment that already exists for ME/CFS

from the summary;
This treatment actually already exists for ME/CFS and patients have been successfully treated with it without a scientific explanation
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I was taken aback, really taken aback by this statement, that a treatment already exists. WE all know of very sick patients, some relatively well to-do, and one would think they would have access. I have never come across anyone who was seriously ill who has recovered. So, until this day I am quite rattled by that statement. Who are these patients who have been successfully treated? Where are they? Forgive me for being so agitated, but there are millions of sick people, thousands upon thousands of tormented parents watching their children suffer. What is this treatment??
 
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Sizzle

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perrier said:
I was taken aback, really taken aback by this statement, that a treatment already exists. WE all know of very sick patients, some relatively well to-do, and one would think they would have access. I have never come across anyone who was seriously ill who has recovered. So, until this day I am quite rattled by that statement. Who are these patients who have been successfully treated? Where are they? Forgive me for being so agitated, but there are millions of sick people, thousands upon thousands of tormented parents watching their children suffer. What is this treatment??
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Been a couple of weeks since I listened to the podcast, but I do remember him saying this and to me it came across as if the people who are trying this where stopping to soon
 
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