According to a widely supported but unproven concept, the autoimmune mechanisms that drive neuroinflammation in multiple sclerosis (MS) are triggered by virus infection. However, a direct viral trigger of MS has not been identified. MS models in non-human primates suggest that lifelong asymptomatic infection with certain herpesviruses (e.g. cytomegalovirus) creates a repertoire of potentially autoreactive memory T cells. When these are exposed to antigens released after central nervous system injury as a consequence of an unknown pathogenic event, they are reactivated and induce autoimmune neurological disease. This response-to-damage of antiviral memory cells can take place years after the initiating infection. Consequently, elucidating the anti-herpesvirus T-cell repertoire might provide new targets for preventive diagnosis and therapy.

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Persistent URL dx.doi.org/10.1016/j.molmed.2009.04.001, hdl.handle.net/1765/24474
Citation
't Hart, B., Hintzen, R.Q., & Laman, J.D.. (2009). Multiple sclerosis - a response-to-damage model. Trends in Molecular Medicine, 15(6), 235–244. doi:10.1016/j.molmed.2009.04.001