Study overturns current ideas on how viruses trigger autoimmunity (the molecular mimicry theory), and proposes new theory based on B-cell mutations

[Hip]

A new study from Australia appears to overturn the current theory of how viruses trigger autoimmunity (the molecular mimicry theory), and proposes an entirely new theory, based on genome mutations occurring in B-cells.

If this new understanding of virally-triggered autoimmunity is correct, it could eventually revolutionise autoimmune disease treatment.

Article: here. Study: here.

 

[cfs since 1998]

Fair to point out this is work was only done on people with Hepatitis C Virus. Will take more research to find out if the same mechanism applies to other viruses.

Btw, Hepatitis C was associated with ME/CFS in a 2012 study by the National Cancer Institute (Chang et. al.).

 

[kushami]

I was reading about cryoglobulinemic vasculitis the other day, although I can’t remember where. It was a story about a teacher who had it, and she really struggled with it despite living in a warm place because she couldn’t be in air conditioning, for instance. Had to give up work.

https://dermnetnz.org/topics/cryoglobulinaemia

 

[Treeman]

A good read. It could explain at least a sub set, but also how many get an initial infection but symptoms persist after the infection has disappeared. It brought to mind the few who recovered after rituximab treatment.

It says they’ve found it in 4 individuals, but how many individuals did they look at? Thanks.

 

[Hip]

I wonder whether there is an ongoing mechanism by which the persistent viral infection is constantly creating these mutated B-cells. The model used in the study is hepatitis C virus triggering the autoimmune disease cryoglobulinemic vasculitis.

This autoimmune disease often (but not always) goes into remission after the hepatitis C virus is fully eliminated with antivirals. See: this study.

So that suggests the autoimmune disease is being maintained by the viral infection in many cases, and once the infection is cleared, so is the autoimmunity. This would imply that the infection is constantly creating mutated B-cells.

So if researchers could figure out the mechanism by which the viral infection is creating these mutated B-cells, you might be able to target that mechanism with drugs, in order to stop these B-cells from being created. In most cases, we do not have antivirals or antimicrobials which can fully eliminate the infection, but if you can prevent the infection creating mutated B-cells, that might halt the autoimmunity.

 

[bad1080]

So that suggests the autoimmune disease is being maintained by the viral infection in many cases, and once the infection is cleared, so is the autoimmunity. This would imply that the infection is constantly creating mutated B-cells.

can hep.c "hide" in the CNS like EBV does?

 

[Hip]

can hep.c "hide" in the CNS like EBV does?

Perplexity.ai says that hepatitis C virus can infect the CNS.