Researchers at Stanford published evidence connecting Epstein‑Barr virus infection to the development of systemic lupus erythematosus. The study demonstrated that EBV can reprogram B cells to produce autoantibodies and sustain autoimmune responses, providing mechanistic support for a decades‑long epidemiological association. The work, appearing in Science Translational Medicine, used molecular and immunologic assays to show viral‑driven changes that plausibly initiate and perpetuate lupus pathology. Authors suggested the findings could guide vaccine or antiviral strategies aimed at preventing or modifying disease onset. If corroborated in larger cohorts, the discovery may redirect therapeutic strategies toward viral prevention and open new avenues for lupus interception trials.