Study pinpoints how Epstein-Barr virus triggers multiple sclerosis
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Biologists have identified the mechanism by which Epstein-Barr virus (EBV) triggers multiple sclerosis (MS), according to a study published in Nature on July 15. The findings resolve a decades-old medical mystery, linking EBV infection directly to the autoimmune attack on myelin. The discovery opens new avenues for MS prevention and treatment.
The Mechanism
Researchers at the University of California, San Francisco, and the University of Cambridge found that EBV produces a protein called EBNA2 that mimics a human protein involved in myelin production. This molecular mimicry causes immune cells to attack both the viral protein and the human myelin basic protein, leading to demyelination. The study analyzed blood samples from over 1,000 MS patients and 2,000 healthy controls, confirming the cross-reactivity in 95% of MS cases.
Clinical Implications
The discovery suggests that existing antiviral drugs against EBV could be repurposed to prevent MS in high-risk individuals. A clinical trial testing the antiviral valacyclovir in 300 patients with early MS symptoms is set to begin in September 2026. Additionally, a vaccine targeting EBNA2 is in preclinical development at the National Institutes of Health.
What's Next
The valacyclovir trial is expected to report initial results by late 2027. It remains unclear whether the vaccine approach will succeed in humans, as previous EBV vaccines have failed to prevent infection.
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Study pinpoints how Epstein-Barr virus triggers multiple sclerosis
