How a Virus Nearly Everyone Carries Triggers Multiple Sclerosis

For decades, scientists knew Epstein-Barr virus was linked to MS. Now they know exactly how it flips the switch.

Epstein-Barr virus (EBV) is one of the most common viruses on Earth — roughly 90% of the global population carries it. For most people, the infection remains harmless for life. But for a small subset, EBV has long been known as a primary trigger for multiple sclerosis (MS), a chronic autoimmune disease that attacks the protective myelin sheath around nerves, affecting 2.9 million people worldwide.

What was missing until now was the mechanism — the exact biological chain reaction that turns a harmless virus into a catalyst for neurological destruction. A team led by Dr. Natalia Drosu at Massachusetts General Hospital has finally filled that gap, publishing their findings in Science Translational Medicine on July 15, 2026.

The CD4+ T Cell Connection

The researchers discovered that immune T-cell activity is twice as high in people with MS as in healthy individuals. When they systematically removed different types of T cells from the participants, they found that the immune system's response to EBV dropped dramatically once a specific type — CD4+ T cells — was taken out of the equation. This pinpointed CD4+ T cells as the primary driver of the autoimmune attack.

This finding was reinforced by an existing MS drug called frexalimab, which acts directly on CD4+ T cells. The drug reduces inflammation and nerve damage by blocking the activity of these cells, and the new study explains why it works: it interrupts the EBV-triggered immune cascade at its source.

Anti-CD20 Therapies: A Second Path

The team also investigated a class of drugs called anti-CD20 therapies, which are already used to treat MS. They measured CD4+ T cell levels in 60 MS patients before and six months after starting anti-CD20 treatment. The results showed that these therapies also reduce the immune system's responsiveness to EBV, though through a different pathway than frexalimab.

Together, these findings suggest that clinicians may soon have a clearer, mechanism-based strategy for choosing which immunotherapy to prescribe for which patient — a step toward personalized treatment for MS.

What This Means

MS currently has no cure. Available drugs can slow progression and reduce the frequency of relapses, but they work differently for different patients. Understanding the precise molecular mechanism by which EBV triggers the disease opens the door to therapies that could prevent MS from developing in the first place — particularly for people who show early signs of the condition.

The study also raises an intriguing question: if a virus carried by 90% of people triggers MS in only a fraction of carriers, what else must be going on? The answer likely involves genetic predisposition, additional environmental factors, and the timing of the initial infection — all areas that now have a clearer roadmap for investigation.

— A knowledge brief from X5H, based on findings published in Science Translational Medicine, July 2026.