Autoimmunity as a Consequence of Retrovirus-Mediated Expression of C-FLIP in Lymphocytes

[Overstressed]

I have no access to the full article, but the abstract is interesting to say the least. It describes the expression of a protein and the accumulation of activated B-cells.

It's interesting in the context of what Dr. Ian Lipkin said in the press-conference, i.e., polyclonal activation of B-cells...

Here's the abstract:
http://www.cell.com/immunity/abstract/S1074-7613(00)80150-8


Best regards,
OS.

 

[alex3619]

c-FLIP can also be initiated by LPS (lipopolysaccharide) and NFkB I think, though I would have to do some reading to be sure. Both LPS and NFkB appear to be elevated in ME. So this fits with known ME and CFS biochemistry. Bye, Alex

 

[lansbergen]

http://www.ncbi.nlm.nih.gov/pubmed/21871974

Autoimmune disease: A role for new anti-viral therapies?

Dreyfus DH.
Source

Pediatrics, Yale University School of Medicine, New Haven, CT, United States. dhdreyfus@pol.net
Abstract

Many chronic human diseases may have an underlying autoimmune mechanism. In this review, the author presents a case of autoimmune CIU (chronic idiopathic urticaria) in stable remission after therapy with a retroviral integrase inhibitor, raltegravir (Isentress). Previous reports located using the search terms "autoimmunity" and "anti-viral" and related topics in the pubmed data-base are reviewed suggesting that novel anti-viral agents such as retroviral integrase inhibitors, gene silencing therapies and eventually vaccines may provide new options for anti-viral therapy of autoimmune diseases.
Cited epidemiologic and experimental evidence suggests that increased replication of epigenomic viral pathogens such as Epstein-Barr Virus (EBV) in chronic human autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus Erythematosus (SLE), and multiple sclerosis (MS) may activate endogenous human retroviruses (HERV) as a pathologic mechanism.
Memory B cells are the reservoir of infection of EBV and also express endogenous retroviruses, thus depletion of memory b-lymphocytes by monoclonal antibodies (Rituximab) may have therapeutic anti-viral effects in addition to effects on B-lymphocyte presentation of both EBV and HERV superantigens. Other novel anti-viral therapies of chronic autoimmune diseases,
such as retroviral integrase inhibitors, could be effective, although not without risk.