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Updated: Jun 11, 2026

A Model for Epilepsy of Infectious Etiology using Theiler's Murine Encephalomyelitis Virus
05:33

A Model for Epilepsy of Infectious Etiology using Theiler's Murine Encephalomyelitis Virus

Published on: June 23, 2022

Different strains of Theiler's murine encephalomyelitis virus antagonize different sites in the type I interferon

Spyridon Stavrou1, Zongdi Feng, Stanley M Lemon

  • 1Committee of Microbiology, the University of Chicago Medical Center, 5841 S. Maryland Ave., Chicago, Illinois 60637, USA.

Journal of Virology
|July 9, 2010
PubMed

Insights

Theiler

Area of Science:

  • Virology
  • Neuroimmunology
  • Molecular Biology

Background:

  • Theiler's murine encephalomyelitis virus (TMEV) causes central nervous system demyelination.
  • DA TMEV induces persistent infection and demyelinating disease, a model for multiple sclerosis.
  • GDVII TMEV causes acute encephalitis without persistence.

Purpose of the Study:

  • To investigate the mechanism by which Cardiovirus L protein inhibits beta interferon (IFN-beta) gene transcription.
  • To determine how different TMEV strains (DA and GDVII) utilize L protein to modulate the IFN-beta pathway.
  • To understand the role of L protein in viral persistence and disease pathogenesis.

Main Methods:

  • Analysis of IFN-beta gene transcription in infected cells and mice.
  • Investigation of the interaction between viral L protein and host interferon regulatory factor 3 (IRF-3) signaling pathway components.
  • Comparison of L protein function between DA and GDVII TMEV strains.

Main Results:

  • Both DA L and GDVII L proteins inhibit IFN-beta gene transcription by interfering with IRF-3 activation.
  • DA L blocks IFN-beta transcription downstream of MAVS but upstream of IRF-3 activation.
  • GDVII L acts downstream of IRF-3 activation.
  • Persistent DA TMEV infection is associated with low levels of IFN-beta mRNA in the CNS.

Conclusions:

  • Cardiovirus L protein differentially regulates the IRF-3 signaling pathway, impacting viral persistence and disease.
  • The specific inhibition point of DA L protein may contribute to viral persistence and restricted viral protein expression in chronic demyelinating disease.
  • Understanding these mechanisms provides insights into viral pathogenesis and potential therapeutic targets for TMEV-induced diseases.

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