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Mechanisms of viral pathogenesis in rheumatic disease
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Introduction |
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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.1 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.2 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
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