EBV's Role in Lupus Pathogenesis: Insights from Stanford Research

A Stanford-led study demonstrates that Epstein-Barr virus (EBV) infection reprograms B cells into a defined driver phenotype linked to systemic lupus erythematosus (SLE). EBV-infected B cells were markedly more prevalent in lupus patients and are highlighted as candidate therapeutic targets.

Using high-precision sequencing, investigators compared B cells from patients and healthy controls, focusing on infected-cell frequency and transcriptional and epigenetic state as primary endpoints. The team reports that EBV-infected B cells were significantly more frequent in patients. Sequencing identified consistent transcriptional and epigenetic differences across cohorts, supporting reproducible cohort-level distinctions.

At the molecular level, EBV redirects B-cell programs toward a reproducible "driver" phenotype with distinct signatures: transcriptional shifts favoring immune-activating pathways, epigenetic remodeling consistent with persistent activation, and marker patterns compatible with autoreactive potential. These changes were observed across multiple assays and sample sets, linking the molecular phenotype to increased autoimmune potential in affected B cells.

The higher proportion of EBV-infected B cells in patients offers a plausible pathophysiologic explanation for the epidemiologic association between EBV exposure and lupus and strengthens the mechanistic connection—without implying immediate diagnostic utility.