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Characterization of coronavirus JHM variants isolated from Wistar Furth rats with a viral-induced demyelinating

V L Morris1, C Tieszer, J Mackinnon

  • 1Department of Microbiology and Immunology, University of Western Ontario, London, Canada.

Virology
|March 1, 1989
PubMed

Insights

Murine hepatitis virus (MHV) variants isolated from rats show distinct neurological disease patterns. One variant with a peplomer glycoprotein deletion causes chronic demyelination and replicates well in glial cells.

Area of Science:

  • Virology
  • Neuroscience
  • Immunology

Background:

  • Murine hepatitis virus (MHV), specifically the JHM strain (MHV-JHM), causes varied neurological diseases in rats depending on age at inoculation.
  • MHV-JHM causes acute encephalitis in young rats and chronic demyelinating disease in older rats.
  • Wild-type MHV-JHM replicates efficiently in mouse fibroblasts but poorly in glial cells, without forming syncytia.

Purpose of the Study:

  • To isolate and characterize MHV-JHM viral variants from rats with demyelinating disease.
  • To investigate the relationship between viral variant characteristics and induced neurological disease.
  • To understand the role of viral genetic variations in MHV pathogenesis.

Main Methods:

  • Isolation and characterization of three MHV-JHM viral variants from the central nervous system of infected rats.
  • Intracerebral inoculation of Wistar Furth rats of different ages with isolated variants.
  • Analysis of viral-specific mRNA patterns and syncytia formation in glial cell lines (G26-24).

Main Results:

  • Three MHV-JHM variants with distinct mRNA patterns were isolated.
  • One variant, ATllf cord virus, exhibited a deletion in the peplomer glycoprotein mRNA, induced chronic demyelinating disease, and formed syncytia, replicating well in G26-24 cells.
  • Two other variants, ATllf brain virus and ATlle brain virus, lacked this deletion, caused acute encephalitis, and showed reduced replication in G26-24 cells without syncytia formation.

Conclusions:

  • The peplomer glycoprotein deletion in MHV-JHM variants is associated with altered neurovirulence, leading to chronic demyelination and enhanced glial cell tropism.
  • Viral variants can emerge with distinct biological properties, influencing the outcome of MHV-JHM infection in the central nervous system.
  • Understanding these viral variants provides insights into the mechanisms of MHV-induced demyelinating diseases.

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