The immune response to cytomegalovirus and Epstein-Barr virus in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown aetiology. Both genetic and environmental factors are known to contribute to disease development. Pathogenesis involves the production of autoantibodies, and the formation of immune complexes, leading to inflammation and destruction of autologous tissue. SLE is a heterogeneous disease both longitudinally and between affected individuals, and is characterised by periods of exacerbation, known as flares, and periods of remission. The ubiquitous human herpes viruses, cytomegalovirus (HCMV), and Epstein-Barr virus (EBV) have been associated with disease by a variety of mechanisms. Data compiled here suggests SLE patients have elevated IgG responses to HCMV and EBV, but unlike healthy controls these responses do not accumulate with age. No association has been found between the carriage of these viruses, or the magnitude of response against these viruses, and any clinical measurements of disease activity. EBV load is 5.4 times higher in SLE patients than controls. Azathioprine treatment is associated with a 4.4 fold rise in EBV load, no other drugs show associations with EBV load. Among SLE patients EBV load is inversely correlated with CD8+ T-cell IFN\(\gamma\) responses, suggesting impaired T-cell responses are the cause of elevated load. HCMV seropositivity is associated with a 7-year delay in development of disease among SLE patients, and a reduction in plasma IFN\(\alpha\) concentration