Epstein-Barr virus antibodies plus genetic factors raise MS risk

A new study has found that antibodies targeting the Epstein-Barr virus (EBV) may mistakenly attack proteins in the brain, offering fresh insight into how EBV is linked to multiple sclerosis (MS).

Researchers also discovered that both EBV-targeting antibodies and a person’s genetics independently contribute to MS risk. People with specific EBV antibodies and genetic traits associated with MS are at a significantly higher risk of developing the condition.

EBV, which causes infectious mononucleosis (or “mono”), is a widespread virus—most people are infected by adulthood without even knowing it. While previous research has confirmed EBV as a key risk factor for MS, the exact mechanism behind this link has remained unclear. One possible explanation is molecular mimicry, where the immune system’s response to EBV mistakenly harms healthy brain cells.

Scientists have long suspected that an EBV protein called EBNA1 closely resembles a brain protein known as GlialCAM. This study, which analysed antibody profiles from 650 people with MS and 661 people without, found that MS patients were significantly more likely to have antibodies targeting EBNA1. These antibodies were also more likely to attack GlialCAM, supporting the molecular mimicry theory.

Beyond EBV infection, genetics also play a role in MS risk. A genetic variant called HLA-DRB1*15:01 is a well-known MS risk factor, while another variant, HLA-A*02:01, appears to be protective. The study found that people with both EBV-targeting antibodies and the HLA-DRB115:01 variant were more than nine times as likely to develop MS. Those who lacked the protective HLA-A02:01 variant had an even greater risk.