Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and multiple sclerosis (MS) are complex autoimmune inflammatory diseases influenced by genetic, environmental and infectious agents like Epstein-Barr virus (EBV). EBV has been proposed to impact immune pathways through molecular mimicry, diverting antibody reactivity towards host tissues. This review explores the literature on EBV-specific similarities with human peptides and cytokines that might contribute to the onset of RA, SLE and MS. In conclusion, it is vital to conduct experimental computational analyses focusing on the homology between EBV and human proteins to unravel the complexities of autoimmune diseases and advance therapeutic approaches. These insights highlight the significance of collaborative efforts and diverse clinical studies for validation, linking the gap between research and practical applications in the complex field of autoimmunity.

Keywords: Epstein–Barr virus; aetiological agents; antigenic determinant; autoimmunity; molecular mimicry; multiple sclerosis; self‐tolerance; systemic lupus erythematosus.

© 2025 The Scandinavian Foundation for Immunology.