«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.» Dette er å lese i pubmed her.
Men kan dette egentlig ha sin årsak i XMRV og andre gammarelaterte retrovirus i samme familie – og ikke HERVs? Uansett denne publikasjonen lansert online 18 august 2011 ser både spennende og interessant ut. Den tar med en rekke ulike terapier for autoimmune sykdommer og en rekke kjente patogener for ME og andre neuroimmunologiske sykdommer.
Abstraktet som står i teksten under her finnes du her:
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.
Keywords: Chronic autoimmune urticaria; Epstein–Barr Virus Infection; HIV-1; HERV; Immunopathology; Vaccines; RNAse P EGS; RNAi; Rheumatoid Arthritis; Systemic Lupus Erythematosus; Multiple sclerosis; XLP
Abbreviations: CMV, Cytomegalovirus; EBV, Epstein–Barr Virus; HSV, Herpes Simplex; HIV-1, Human Immunodeficiency Virus 1; VZV, Varicella-Zoster Virus; HSV6, Human Herpes Virus 6; ANA, Antinuclear Antibody; MS, Multiple Sclerosis; EGS, RNAse P External Guide Sequence; RNAi, Interfering RNA; RAG, Recombination Activating Genes; RA, Rheumatoid Arthritis; SH2D1A, Sarc Homology 2 Domain protein 1A; SAP, SLAM-Associated Protein; SLE, Systemic Lupus Erythematosus; XLP, X-linked Lympho-Proliferative syndrome; ERV, Endogenous Retro Virus; HERV, Human Endogenous Retro Virus
1. Rational for anti-viral therapy of autoimmune disease
1.1. Chronic idiopathic urticaria, a prototype for the role of anti-viral therapy in autoimmune syndromes
1.2. A case of steroid, cyclosporine and xolair resistant chronic autoimmune urticaria with response to anti-viral therapy, raltegravir
2. Overview of immunopathology associated with Epstein–Barr Virus (EBV)
2.1. Epstein–Barr Virus infection as a model of epigenomic chronic viral infection associated with human immunopathology and autoimmune disease
2.2. X-linked lympho-proliferative syndrome as a model of viral induced immunopathology
3. Abnormal immune responses to EBV infection in prototypical autoimmune diseases
3.1. Rheumatoid Arthritis (RA)
3.2. Systemic Lupus Erythematosus (SLE)
3.3. Multiple Sclerosis (MS)
3.4. Epigenomic pathogens (such as EBV) and endogenous viral pathogens (HERV) as triggers to lymphocyte activation and epitope spreading
4. Evidence based medicine supporting anti-viral therapy for autoimmune diseases
4.1. Memory B lymphocytes as targets for anti-viral therapy in autoimmune disease
4.2. Retroviral integrase inhibitors as a novel form of anti-viral therapy for autoimmune disease
4.3. Other forms of novel anti-viral therapy of autoimmune disease
5. Anti-viral therapy of autoimmune diseases: conclusions