Untreated multiple sclerosis patients showed EBV-specific CD4+ T-cell responses about twice as strong as healthy controls, pinpointing a measurable immune pathway tied to the disease.
The study found those cells mainly targeted EBV capsid and glycoprotein antigens, while responses to other herpes viruses stayed similar, sharpening the case for an EBV-specific mechanism.
Anti-CD20 B-cell depletion cut the EBV-directed response 2.5-fold across two MS groups totaling 69 patients and eliminated detectable viral shedding in saliva.
Published in Science Translational Medicine, the findings suggest current MS drugs may work partly by disrupting EBV reservoirs and could guide EBV-targeted vaccines, antivirals and treatment monitoring.
A common virus triggers MS. With vaccine trial results due this year, could we soon prevent this devastating neurological disease?
If a virus fuels multiple sclerosis, will future treatments target the infection instead of suppressing the entire immune system?
Unraveling the 32-Fold MS Risk: How Epstein-Barr Virus Drives Multiple Sclerosis and the Race for Targeted Prevention
Overview
A major breakthrough in Multiple Sclerosis (MS) research was announced in July 2026, revealing how the Epstein-Barr virus (EBV) triggers the immune response that leads to MS. Scientists have identified specific EBV antigens involved in the disease process, marking a pivotal step for drug development. This detailed understanding offers a clearer roadmap for creating targeted therapies that address the root cause of MS, rather than just managing symptoms. The findings open new possibilities for more precise treatments and guide future research towards innovative approaches for MS prevention and care.