Epstein-Barr virus (EBV) is proposed as the mechanistic thread connecting genetic susceptibility, immune dysfunction, and clinical phenotype in multiple sclerosis.
This model provides a mechanistic framework linking genetic risk to immune pathology in multiple sclerosis through Epstein-Barr virus infection.
Multiple Sclerosis and Epstein-Barr Virus: Genetics, BACH2, and CD8 Failure in a Convergent Model. Integrating transcriptomic, genetic, and mechanistic evidence. Analysis date: 31 May 2026. Data sources: GSE21942 (55 MS + 37 HC), GSE108000 (scRNA-seq, 130K cells), GSE166106 (CD8/memory), IMSGC GWAS. This preprint presents a convergent model incorporating Epstein-Barr virus (EBV) as the mechanistic thread connecting genetic susceptibility, immune dysfunction, and clinical phenotype in MS. The central hypothesis is that EBV simultaneously disables CD8-mediated control through viral immune evasion mechanisms, hijacks B cell activation through latent proteins (EBNA2, LMP1), and drives the inflammatory loop that sustains disease activity. Without EBV, core phenomena in MS lack a mechanistic framework linking genetic risk to immune pathology.
Javier Martínez Mellado (2026) conducted a review in Multiple Sclerosis. Epstein-Barr virus (EBV) was evaluated. Epstein-Barr virus (EBV) is proposed as the mechanistic thread connecting genetic susceptibility, immune dysfunction, and clinical phenotype in multiple sclerosis.