Theiler's Murine Encephalomyelitis Virus-Induced Demyelinating Disease (TMEV-IDD) and Autoimmunity

Emily M.L. Chastain, Stephen D Miller*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations


Theiler's murine encephalomyelitis virus-induced demyelinating disease is a CD4+ T-cell-mediated model of multiple sclerosis. Life-long persistent viral infection of antigen-presenting cells and glial cells residing in the central nervous system (CNS) is directly related to the development of the chronic demyelinating disease. Initial myelin damage is mediated by a bystander mechanism wherein the primary effector cells are mononuclear phagocytes (microglia/macrophages) activated by inflammatory cytokines produced from Theiler's murine encephalomyelitis virus-specific T cells responding to viral epitopes that persist in the CNS. Early myelin destruction leads to the de novo activation of myelin-specific T cells (epitope spreading). The initial myelin response is directed towards the immunodominant proteolipid protein 139-151 epitope, and epitope spreading then leads to an ordered progression of T-cell responses to multiple myelin autoepitopes, which play a significant role in the chronic phase of the disease by escalating the demyelinating process. The continuous presence of the virus within the CNS perpetuates this chronic inflammatory process in which epitope spreading leads to the induction of autoreactive T cells.

Original languageEnglish (US)
Title of host publicationInfection and Autoimmunity
PublisherElsevier Inc
Number of pages12
ISBN (Print)9780444632692
StatePublished - Jan 1 2015


  • Autoimmune disease
  • Bystander damage
  • Central nervous system
  • Epitope spreading
  • Molecular mimicry
  • Multiple sclerosis
  • Theiler's virus
  • Virus infection

ASJC Scopus subject areas

  • Medicine(all)
  • Immunology and Microbiology(all)

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