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Article Abstract

BackgroundSystemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by the production of autoantibodies that target most of the organ systems and lead to their dysfunction. The exact etiology of SLE remains unclear; however, genetic and environmental factors are believed to play significant roles. Viral infections, particularly Epstein-Barr virus (EBV), have been implicated as environmental triggers in SLE pathogenesis however, the observations remained inconsistent among studies and populations. The present study uses a meta-analysis approach to explore the prevalence of EBV infection in the general population and their role in the pathogenesis of SLE.Materials and MethodsVarious databases such as PubMed, Scopus, and ScienceDirect were searched to obtain eligible studies based on predetermined inclusion and exclusion criteria. The Newcastle-Ottawa Scale (NOS) was used for quality assessment of the eligible studies, and Comprehensive Meta-Analysis (CMA) v4 software was used for the analysis. Publication bias was assessed with funnel plots and Egger's regression, while heterogeneity was evaluated with Cochrane Q and I statistics.ResultsIn the present investigation, a total of 28 studies comprising of 3926 healthy controls and 2968 SLE patients were included. EBV infections were prevalent in the healthy controls. While comparing the frequency of EBV DNA or antibodies positivity, the SLE patients had a higher positivity rate than the healthy controls, indicating that EBV infection is a risk factor for developing SLE. Furthermore, the sensitivity analysis also revealed that the meta-analysis was robust.ConclusionThe majority of healthy subjects were previously exposed to EBV, and the infection could be a potential risk factor in SLE pathogenesis. However, future research is required to elucidate the possible mechanisms of EBV reactivation in SLE patients and examine potential preventive measures, such as antiviral therapies, in mitigating SLE risk.

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http://dx.doi.org/10.1177/09612033251371333DOI Listing

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