Herpesvirus infection, in particular EBV infection, has been implicated in several major autoimmune diseases, including systemic lupus erythematosus (SLE), multiple sclerosis (MS) and rheumatoid arthritis (RA). Herpesvirus infection has potential roles in both initiating the autoimmune process and exacerbating disease progression. In particular, EBV has a proposed role in initiating the anti-nucleoprotein antibodies that are characteristic of SLE through molecular mimicry. There is also evidence to suggest that there is productive infection with EBV in the brain lesions of MS patients and in the synovium of RA patients. Research has been conducted in a mouse gamma-herpesvirus model, as it serves as a useful model for productive infection within autoimmune target tissues. The novel mechanisms by which EBV could contribute bystander effects by amplification of innate immune responses, along with preclinical and epidemiological studies into the role of herpesviruses in SLE, MS and RA, and clinical studies into the potential benefit of antiviral therapy, are discussed in this review.
