Researchers at the University of Zurich have uncovered how the Epstein-Barr virus (EBV) and a genetic risk factor interact to trigger multiple sclerosis (MS), providing new insight into the mechanisms behind this autoimmune disease. The findings highlight the combined influence of environmental and genetic factors in disease onset and suggest potential avenues for targeted therapies.
While EBV infection is nearly universal—95 percent of healthy people carry the virus—it alone does not cause MS. Infection during late adolescence, particularly if symptomatic as infectious mononucleosis, significantly increases MS risk. The new study, conducted in collaboration with teams in China, Germany and the UK, focused on the interaction between EBV and the HLA-DR15 haplotype, a gene variant strongly associated with MS.
HLA-DR15 molecules, found on immune cells, act as receptors that guide T cells in recognising viral components. EBV infects B cells, where it persists lifelong. In individuals carrying HLA-DR15, the immune response can mistakenly target not only EBV but also the body’s own myelin proteins. EBV-infected B cells produce myelin fragments that are presented alongside HLA-DR15, activating T cells that then attack the protective myelin sheath surrounding nerve fibers. This autoimmune attack leads to demyelination and a range of neurological symptoms, including paralysis, visual impairment and fatigue.
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The study illustrates how a combination of viral infection and genetic susceptibility can trigger the autoimmune processes central to MS. The findings also underscore the potential of EBV-targeted strategies, including vaccines, as a means of preventing or mitigating MS. EBV is implicated not only in MS but also in other autoimmune diseases, such as rheumatoid arthritis and systemic lupus, and in certain cancers.
Understanding these mechanisms may help guide the development of future therapies aimed at interrupting the harmful interactions between EBV, B cells, and T cells, potentially reducing the onset or progression of MS.
This news item has been summarised using AI and checked by humans before publication.
Sources
University of Zurich
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