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Murine coronavirus delays expression of a subset of interferon-stimulated genes

Kristine M Rose1, Ruth Elliott, Luis Martínez-Sobrido

  • 1Department of Microbiology, University of Pennsylvania, School of Medicine, 36th Street and Hamilton Walk, Philadelphia, PA 19104-6076, USA.

Journal of Virology
|April 2, 2010
PubMed

Insights

Mouse hepatitis virus (MHV) resists type I interferon (IFN-I) antiviral effects by delaying interferon-stimulated gene induction. MHV inhibits an alternative IFN-I pathway, not the main signaling cascade, impacting IRF-3 function.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Type I interferons (IFN-I) are crucial for controlling viral infections, including coronaviruses.
  • Mouse hepatitis virus (MHV) exhibits cell-type-dependent resistance to IFN-I antiviral activity.
  • Previous studies show MHV replication is inhibited by IFN-I in primary cells but less so in cell lines.

Purpose of the Study:

  • To investigate the mechanisms by which MHV resists IFN-I-mediated antiviral responses.
  • To determine if MHV interferes with interferon-stimulated gene (ISG) induction.
  • To elucidate the specific IFN-I signaling pathways affected by MHV infection.

Main Methods:

  • Infection of cell lines (L2, 293T) and primary cells (macrophages, fibroblasts) with MHV.
  • Treatment with IFN-alpha/beta and superinfection with other RNA viruses (SeV, TMEV, VSV, NDV).
  • Analysis of ISG induction, STAT1-STAT2 phosphorylation, nuclear translocation, and IRF-3 activity.

Main Results:

  • MHV infection delays ISG induction triggered by SeV or IFN-beta when MHV infection precedes exposure.
  • MHV does not block the canonical IFN-beta signaling pathway involving STAT1-STAT2 phosphorylation.
  • MHV partially inhibits IRF-3-dependent transcription, suggesting interference with an alternative IFN-I pathway.

Conclusions:

  • MHV employs a mechanism to evade IFN-I antiviral effects by delaying ISG induction through an alternative pathway.
  • The virus appears to interfere with early ISG induction, potentially by modulating IRF-3 function.
  • Understanding this evasion strategy is critical for developing effective antiviral therapies against coronaviruses.

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