Epstein–Barr virus and autoimmunity: the role of a latent viral infection in multiple sclerosis and systemic lupus erythematosus pathogenesis

Multiple sclerosis (MS) and systemic lupus erythematosus (SLE) are both chronic autoimmune diseases with unknown etiology. To date, EBV is the most closely implicated infectious agent to be associated with both MS and SLE. Epidemiological findings show a strong correlation between EBV infection and the risk of developing these diseases. The type and magnitude of both EBV-specific antibodies and T-cell responses produced by MS or SLE patients are dysregulated when compared with healthy cohorts. Despite all these findings, it is still not clear if and how EBV triggers autoimmunity. EBV infects and establishes latency mainly in B cells, but it can also infect other cell types and indirectly influence the activation status of the immune system by stimulating the production of proinflammatory mediators. This could play a role in both MS and SLE pathogenesis. In this review we will summarize recent literature that links EBV infection to SLE and MS, and discuss possible new mechanisms that explain how EBV drives autoimmunity