March 11, 2025 | News | Living with MS MS Research MS Treatments

Virus activity may make MS more active

A great deal of MS research is currently focused on the Epstein-Barr virus (EBV) following a report that found that MS rarely developed in people who had not been previously infected with EBV (Bjornevik and colleagues. Science 2022;375:296-301). This suggests that EBV is an important trigger of MS – although how this occurs has not been fully worked out.

EBV is everywhere and most people contract the virus during childhood or adolescence. In most cases there are no symptoms. If acquired later, EBV can cause mononucleosis (‘the kissing disease’). A new study looked at if the risk of developing MS was higher in people who had mononucleosis (Diaz-Decaro and colleagues. ACTRIMS 2025;V465). The results were presented at the Americas Committee for Treatment and Research in MS (ACTRIMS) in February.

The researchers combed through a population database and identified almost 4,721 people who had mononucleosis over a 24-year period. Then they followed them over a six-year period to see if these people were more likely to develop MS.

In the mononucleosis group, the incidence (i.e. number of new cases) was 22.5 per 100,000 population. This is similar to an incidence of 21.57/100,000 that has been reported in other U.S. population studies (Kwon and colleagues. AAN 2024;P11-6.003). In people who didn’t have mononucleosis, the incidence was two-thirds lower – 7.7 per 100,000 population. This suggests that people who develop mononucleosis during their teen years have a three-fold higher risk of subsequently developing MS. This raises an important question: would preventing EBV infection (with a vaccine) reduce the number of people who develop MS?

Another question is how EBV contributes to the MS disease process. EBV infects a type of immune cell (B cells) and one theory is that these infected B cells cause inflammation and damage to nerve tissue. A new study looked at B cells and found that people with MS had a higher viral load in their B cells than people without MS (Thebault and colleagues. ACTRIMS 2025;P467). The virus was also more active in people with MS – and these periods of high viral activity matched up with periods of disease activity (i.e. relapses and lesions seen on MRI). Higher viral loads also meant more MS activity over time.

A separate study looked at this issue from another angle (King and colleagues. ACTRIMS 2025;CE1.2). It found that there was a heightened inflammatory signal in the three months before people had an MS relapse. The signal originated primarily from B cells that were responding to a flare-up in EBV activity.

These results suggest that the immune system in people with MS may not be as effective in controlling viral infections, giving EBV a freer rein to cause tissue damage. Or it may be that there is an impairment in how B cells function. Interestingly, some have speculated that the MS medications that target B cells (e.g. Ocrevus and Kesimpta) may be effective, in part, because they eliminate the number of EBV-infected B cells in the body (Phuong and colleagues. Mult Scler Relat Disord 2023:70:104497).

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