Epstein–Barr virus and rheumatoid arthritis

The cause of rheumatoid arthritis (RA) is still unknown. Both genetic and environmental factors may help its development. For 25 years, the Epstein–Barr Virus (EBV) has been suspected to contribute to RA pathogenesis. RA patients have higher levels of anti-EBV antibodies than healthy controls. EBV-specific suppressor T cell function is defective in RA. HLA-DRB1*0404, an RA predisposing allele, is associated with low frequencies of T cells specific for EBV gp110, a replicative phase glycoprotein critical for the control of EBV infection. Patients with RA have higher EBV load in peripheral blood lymphocytes (median 8.84 copies per 500 ng DNA) than healthy controls (median 0.6 copies/500 ng DNA). EBV, a widespread virus, highly recognized by antibodies but never eliminated, is an ideal candidate to trigger chronic immune complex disease. Anti-EBV antibody responses should be considered as one of the chronic autoantibody responses that are most relevant to the development of RA.