Bob
Senior Member
- Messages
- 16,455
- Location
- England (south coast)
This is not a new research paper. It was published in August 2011, but it's fascinating.
Credit goes to 'XMRV Global Action' for posting it on their twitter stream.
I didn't know which sub-forum to post this under, because although it doesn't actually mention ME/CFS, it could almost have been written specifically for ME/CFS. It mentions: autoimmunity; treatment of autoimmune conditions with anti-retrovirals; Rituximab; B-cells; viruses hiding in B-cells; expression of human endogenous retroviruses (HERVs); EBV; B-cells expressing HERVs; and Memory B cells being the reservoir of infection of EBV. Basically, it seems to bring almost all of our current research into ME under a single research paper!
Autoimmune disease: A role for new anti-viral therapies?
David H. Dreyfus
Pediatrics, Yale University School of Medicine, New Haven, CT, United States.
Received 17 July 2011. Accepted 11 August 2011. Available online 18 August 2011.
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.
http://www.sciencedirect.com/science/article/pii/S1568997211001753
Credit goes to 'XMRV Global Action' for posting it on their twitter stream.
I didn't know which sub-forum to post this under, because although it doesn't actually mention ME/CFS, it could almost have been written specifically for ME/CFS. It mentions: autoimmunity; treatment of autoimmune conditions with anti-retrovirals; Rituximab; B-cells; viruses hiding in B-cells; expression of human endogenous retroviruses (HERVs); EBV; B-cells expressing HERVs; and Memory B cells being the reservoir of infection of EBV. Basically, it seems to bring almost all of our current research into ME under a single research paper!
Autoimmune disease: A role for new anti-viral therapies?
David H. Dreyfus
Pediatrics, Yale University School of Medicine, New Haven, CT, United States.
Received 17 July 2011. Accepted 11 August 2011. Available online 18 August 2011.
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.
http://www.sciencedirect.com/science/article/pii/S1568997211001753