ABSTRACT
Background and systemic lupus erythematosus [SLE] is an autoimmune rheumatic disease with no known cure. In predisposed individuals, the initial stimulus is likely to be one or more of the environmental agents interacting with susceptibility genes. For many years, investigators have suspected that Epstein-Barr virus [EBV] might somehow by involved in the aetiopathogenesis of systemic lupus. Studies have examined this possibility from various angles and have arrived at different conclusions. The present work was carried out to evaluate the role of EBV as an environmental risk factor for lupus in our population and to assess the role of this virus in the clinical course of the disease. the study included 25 lupus patients satisfying the American College of Rheumatology criteria for diagnosis of SLE. Twenty age and sex matched healthy subjects were chosen as controls. All patients were subjected to complete history taking and full clinical assessment. Routine laboratory investigations were carried out as well as study of immunologic parameters including antinuclear antibodies, anti-double stranded DNA and complement components C3 and C4. in all study subjects, serology for EBV viral capsid antigen [VCA] IgG was performed using both enzyme linked immunosorbent assay [ELISA] and indirect immunofluorescence assay [IFA]. EBV DNA was detected in peripheral blood mononuclear cells by polymerase chain reaction using primers specific for EBV nuclear antigen-1 gene. Besides, interleukin-10 [IL-10] levels were determined in sera by ELSA. Results and twenty three lupus patients [92%] were positive for EBV DNA compared to 12 control subjects [60%], the difference being statistically significant [p= 0.14]. Virtually all study subjects had seroconverted against EBV. When antibody titres were expressed as the geometric mean titre [GMT] after logarthmic transformation, patients with SLE had a significantly higher GMT compared to control subjects [mean +/- SD 3.46 +/- 0.34 vs 2.93 +/- 0.25, t = 5.12, p < 0.001]. When the anti-VCA titre of lupus patients was correlated with different clinical and laboratory findings, a significant positive correlation was detected with disease activity as measured by SLE disease activity index [SLEDAI], while a significant inverse correlation existed with each of C3 and C4. IL-10 levels in SLE patient were significantly higher than those in controls [mean +/- SD 61.37 +/- 90.65 vs 9.73 +/- 20.33 pg/ml. p = 0.002]. Moreover, elevated IL-10 levels correlated significantly with SLEDAI and with titre of anti-VCA in lupus patients. This study provide evidence that EBV infection contributes to the aetiology and/or pathogenesis of SLE and that the presence of the virus may influence the clinical course of the disease