Overview
- Using a new single‑cell RNA sequencing platform (EBV‑seq), researchers identified rare infected B cells and found a roughly 25‑fold higher frequency in lupus patients (about 1 in 400) than in controls (fewer than 1 in 10,000).
- The team shows EBV prompts production of the viral protein EBNA2, which binds human genes such as ZEB2 and TBX21 to reprogram autoreactive memory B cells into antigen‑presenting, pro‑inflammatory ‘driver’ cells that recruit T cells.
- Study authors argue the mechanism could underlie many or all lupus cases, while independent experts welcome the work but caution that replication, population diversity, and explanations for why most infected people do not develop lupus are still needed.
- The results bolster translational efforts including EBV vaccine development and B‑cell–targeted approaches such as depletion strategies and CAR‑T therapies; the work was partly funded by the Lupus Research Alliance, and co‑authors have formed EBVio Inc.
- Building on earlier evidence linking EBV to multiple sclerosis, the findings raise the possibility of similar pathways in other autoimmune diseases such as rheumatoid arthritis and Crohn’s, which researchers plan to probe with larger cohorts and strain analyses.