What Roles Does EBV Play in Systemic Lupus Erythematosus? A Synthesis of Its Action Mechanisms

Systemic lupus erythematosus (SLE) is a heterogeneous chronic autoimmune disease. Exogenous pathogen infections act as key environmental triggers for autoimmune activation and the development of SLE, with Epstein-Barr virus (EBV) being a particularly prominent one. EBV, a gamma herpesvirus, has been associated with the development of various autoimmune diseases, including SLE, rheumatoid arthritis, Sjögren's syndrome, and multiple sclerosis. Current studies provide sufficient evidence supporting an association between EBV and SLE; however, the specific underlying mechanisms remain unclear. In this review, we summarize the life cycle of EBV, the serological characteristics of EBV infection in SLE patients, and the mechanisms by which EBV evades the host's innate and adaptive immune responses. We also discuss the potential mechanisms through which EBV contributes to the pathogenesis and progression of SLE, as well as the relevant therapeutic strategies and their limitations.