Study: Genetics and virus play key role in multiple sclerosis

2026-01-17 09:03:00, Shëndeti CNA

Genetics appear to help determine who develops multiple sclerosis (MS), two new studies say.

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

"In addition to EBV infection, genetic factors also play a role," lead researcher Roland Martin, a professor of neurology and neuroimmunology at the University of Zurich in Switzerland, said in a press release.

Specifically, the genetics allow immune cells infected by the virus to continue to produce antibodies that target myelin, the protective sheath that covers neurons, the researchers said.

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

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

Everyone who has multiple sclerosis (MS) has been previously infected with the Epstein-Barr virus, the researchers said in their preliminary notes.

However, about 95% of healthy people also carry the virus, raising the question of what else happens that causes multiple sclerosis in some but not all.

For the new study, researchers used laboratory mice to explore the hidden mechanisms of multiple sclerosis, looking specifically at B cells - 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, the researchers said.

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

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

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

"The role of EBV in multiple sclerosis has been quite mysterious for a long time. We have identified a series of events, including EBV infection, that must occur in a clearly defined sequence to cause localized inflammation in the brain," said principal investigator Tobias Derfuss, a research group leader at the University of Basel in Switzerland.

"While this does not fully explain all aspects of multiple sclerosis, it may be the spark that ignites chronic inflammation in the brain," he said in a press release.

Experts largely agree that both B cells and the 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 on how.

“The model that emerges from our team’s work is very simple and therefore very compelling,” he said in a press release. “In short, we suggest that virus-infected B cells cause lesions.”

Martin pointed out the potential benefits of the findings.

"Our study shows how the most important environmental and genetic risk factors can contribute to multiple sclerosis 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./ CNA