In Probing Epstein-Barr Connection, Researchers Find Potential Target to Protect Against Multiple Sclerosis


A subset of natural killer cells may be a potential target for the development of agents protective against MS.

Multiple sclerosis (MS) is a chronic autoimmune disorder in which inflammatory processes destroy the protective myelin sheath around nerves in the brain, spinal cord, and peripheral nervous system. The exact cause of MS is not known. However, it is widely believed that infection with the Epstein-Barr virus may be highly associated with MS pathology.

The Epstein-Barr virus is a herpes virus that infects over 90% of adults worldwide. Infection with the virus causes mononucleosis in 13% to 22% of individuals. Once inside a host, the Epstein-Barr virus remains dormant in memory B cells and may be sporadically reactivated.

Although studies have shown that infection with Epstein-Barr virus is a significant risk factor for developing MS, only a small percentage of people infected with the Epstein-Barr virus develop MS. In a study recently published in the journal Cell, researchers from the Medical University of Vienna investigated factors that may trigger MS in some patients infected with the virus but not others.

Lead author Hannes Vietzen, M.Sc., and his colleagues recruited a cohort of 270 patients with MS and blood tests positive for the Epstein-Barr nuclear antigen 1 (EBNA1) protein. Each participant was matched with a corresponding EBNA1-positive control individual without MS.

Vietzen and his team found that participants with a strong autoreactive immune response to the Epstein-Barr virus and simultaneous inefficient natural killer cell response had an increased risk of developing MS. Consequently, the investigators identified a subset of natural killer cells as a potential target for the development of agents protective against MS.

The authors concluded, “We demonstrate in our study that different specific immune mechanisms protect individuals from MS, despite the presence of cross-reactive EBNA-1-specific immune responses, and provide further insights into the pathogenesis of MS. Our data suggest that there may be additional therapeutic options for the prevention and therapy of MS.”

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