• Posted January 15, 2026

Genetics, Virus Play Key Roles In MS, Studies Suggest

Genetics appear to help determine who develops multiple sclerosis (MS), a pair of new studies says.

A person’s genetics interact with an infection with Epstein-Barr virus (EBV) to cause a severe autoimmune reaction that leads to multiple sclerosis, researchers reported this week in the journal Cell.

“In addition to EBV infection, genetic risk factors also play a role,” senior researcher Roland Martin said in a news release. He’s a professor of neurology and neuroimmunology at the University of Zurich in Switzerland.

Specifically, genetics allow virus-infected immune cells to keep producing antibodies that target myelin, the protective sheath that covers neurons, researchers said.

This autoimmune attack on myelin — and subsequent damage to the nervous system — is a hallmark of multiple sclerosis, researchers said. It causes the paralysis, vision loss and fatigue found in MS.

The results of the two studies add to mounting evidence that Epstein-Barr virus is involved in both causing MS and shaping its progression, researchers said.

Everyone who has MS has previously been infected with Epstein-Barr virus, researchers said in background notes.

However, about 95% of healthy people also carry the virus, raising the question of what else happens to cause MS in some but not all.

For the new study, researchers used lab mice to explore the hidden mechanics of MS, looking specifically at B cells — the immune cells that produce antibodies.

The Epstein-Barr virus can infect B cells, causing them to produce hunter/killer T cell antibodies that target myelin, researchers said.

Normally, these altered B cells would be shut down by strict immune safety mechanisms that kick in before they can cause harm.

But these safety mechanisms are governed by proteins called Human Leukocyte Antigens (HLA), and researchers found that variations in the genes that drive HLA can allow the infected B-cells to continue spinning out of control.

In experimental mice, EBV-infected B cells caused damage to myelin that closely resembled early MS lesions, researchers said.

“The role of EBV in MS has been quite mysterious for a long time. We have identified a series of events including EBV infection that has to happen in a clearly defined sequence to cause localized inflammation in the brain,” said senior investigator Tobias Derfuss, a research group leader at the University of Basel in Switzerland.

“While this is not fully explaining all aspects of MS, it might be the spark that ignites chronic inflammation in the brain,” he said in a news release.

Experts mostly agree that both B cells and Epstein-Barr virus are involved in the disease, but senior researcher Nicholas Sanderson, a project leader at the University of Basel, said there is no consensus about how.

“The model that emerges from the work of our team is very simple and therefore very persuasive,” he said in a news release. “In a nutshell, we suggest that virus-infected B cells cause the lesions.”

Martin pointed to potential benefits from the findings.

“Our study shows how the most important environmental and genetic risk factors can contribute to MS and trigger an autoimmune response that targets myelin components in the brain,” he said.

“Our findings reveal mechanisms that could be targeted by new therapies,” Martin added.

More information

The National MS Society has more on multiple sclerosis.

SOURCES: University of Zurich, news release, Jan. 13, 2026; University of Basel, news release, Jan. 13, 2026