Leader Mechanisms of viral pathogenesis in rheumatic disease

Considerable evidence indicates that viruses may be important environmental factors in the pathogenesis of autoimmune rheumatic diseases. A concordance rate of 25% for the most common illnesses, such as rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) in monozygotic twins shows that genetic factors influence susceptibility to autoimmune diseases. Alternatively, a 70% discordance rate emphasises the importance of environmental factors. Forensic studies of archeological sites revealed the presence of RA-like erosive bony changes in pre-Columbian New World populations dating back 6500 years and the absence of RA in the Old World before the 18th century. This geographical distribution suggests that RA may have spread from the Americas through environmental factors, possibly by a virus, another microorganism, or an antigen. Viruses can elicit acute or subacute and, less often, chronic forms of arthritis. These viral arthritis syndromes can be diagnosed by recognition of well defined clinical signs and detection of viral antibodies and nucleic acids. Viral elements may also play a part in the pathogenesis of idiopathic autoimmune rheumatic diseases. This editorial will assess mechanisms of viral pathogenesis in rheumatic disease by focusing on known viruses capable of causing inflammatory arthritis syndromes and comparing virally induced immunological aberrations with those noted in rheumatic disease patients.