A new theory on autoimmunity with reference to multiple sclerosis.

Recent genetic evidence points towards endogenous retroviruses as playing a pivotal role in the causation of multiple sclerosis and possibly other autoimmune diseases. We discuss various ways in which this association could be brought about. Specifically, we suggest that two endogenous retroviruses, HERV-Fc1 and HERV-K13, on chromosomes X and 19, respectively, contribute to the development of autoimmune T cells by transforming them in multiple sclerosis.

Genetically determined high activity of IL-12 and IL-18 in ulcerative colitis and TLR5 in Crohns disease were associated with non-response to anti-TNF therapy.

Anti-tumour necrosis factor-α (TNF-α) is used for treatment of severe cases of inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC). However, one-third of the patients do not respond to the treatment. A recent study indicated that genetically determined high activity of pro-inflammatory cytokines, including interleukin-1β (IL-1β), IL-6 and interferon gamma (IFN-γ), are associated with non-response to anti-TNF therapy.

[Endogenous retroviruses are associated with autoimmune diseases].

Retroviruses can be transmitted in two fundamentally different ways: 1) They can be horizontally transmitted as infectious virus, or 2) they can integrate in the germ line and be transmitted to offspring and the offsprings' offspring as DNA. The latter is called endogenous viruses. The mode of transmission is called vertical.

Two endogenous retroviral loci appear to contribute to Multiple Sclerosis.

Background: Two endogenous retroviral loci seem to be involved in the human disease Multiple sclerosis (MS).

Results: The two retroviral loci synergize in and contribute to MS (shown by ANOVA). Synergy probably means recombination or complementation of the activated viruses.

Synergy of two human endogenous retroviruses in multiple myeloma.

Multiple myeloma (MM) is a severe, incurable neoplasm of the plasma cells. In this study we have used genetic epidemiology to associate the risk of MM with endogenous retroviral loci in humans. We used SNP analysis on a Sequenom platform and statistical analysis in SPSS.