Multiple sclerosis (MS) is a chronic demyelinating immune-mediated disease of the central nervous system. The aetiology of MS is still unknown, but on the background of genetic susceptibility, both infectious and non-infectious environmental factors can modulate the risk of developing the disease. Among infectious factors, the Epstein Barr virus (EBV) is the most strongly associated with MS. This virus infects human B cells in ∼90% of the general population and virtually 100% of those with MS.
Adults without evidence of remote infection by EBV appear not to develop MS, indicating that such infection may be a prerequisite for disease development. The mechanisms underlying this association, however, have not been clearly elucidated.
A possible mechanism has been described in an article published in the Journal of Immunology by the Clinical Neurology research group led by Dr Bruno Gran in Nottingham. In this study, they propose that EBV alters the ability of B cells to process and present a pathogenetically relevant myelin autoantigen in a way that leads to autoimmunity.
This research could help to better understand the role of EBV infection in MS and try to prevent the disease development.
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