Multiple sclerosis - a response-to-damage model

Trends Mol Med. 2009 Jun;15(6):235-44. doi: 10.1016/j.molmed.2009.04.001. Epub 2009 May 18.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Central Nervous System / immunology
  • Central Nervous System / pathology
  • Central Nervous System / virology
  • Herpesviridae / physiology
  • Humans
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / pathology
  • Multiple Sclerosis / therapy
  • Multiple Sclerosis / virology