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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

Theiler's murine encephalomyelitis virus attachment to the gastrointestinal tract is associated with sialic acid

Ikuo Tsunoda1, Jane E Libbey, Robert S Fujinami

  • 1Department of Pathology, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA.

Journal of Neurovirology
|December 31, 2008
PubMed

Insights

Theiler

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Theiler's murine encephalomyelitis virus (TMEV) exists in several strains, including DA and GDVII.
  • Specific viral protein mutations influence TMEV's interaction with host cells.
  • Sialic acid (SA) is a key molecule in cellular recognition and viral binding.

Purpose of the Study:

  • To investigate the role of sialic acid (SA) in TMEV tropism and infection.
  • To determine how specific TMEV strains and mutants interact with SA-dependent cellular components.
  • To understand the correlation between SA binding and viral persistence.

Main Methods:

  • Neuraminidase treatment of cells to assess SA-dependent infection.
  • Analysis of TMEV strains (DA, GDVII) and mutants (DApB, DApBL2M) with defined genetic modifications.
  • Virus binding assays using intestinal tissue sections to evaluate tropism.

Main Results:

  • Neuraminidase treatment inhibited infection by DA and DApB strains, indicating SA dependence for these viruses.
  • GDVII and DApBL2M strains showed resistance to neuraminidase treatment, suggesting altered SA interactions.
  • All four TMEV variants bound to intestinal goblet cells and mucus in an SA-dependent manner.

Conclusions:

  • Sialic acid (SA) composition on different cell types significantly influences TMEV tropism and infection patterns.
  • Specific viral proteins and mutations dictate the dependence on SA for infection and persistence.
  • Understanding SA-virus interactions is crucial for deciphering viral pathogenesis and host specificity.

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