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Mouse hepatitis coronavirus replication induces host translational shutoff and mRNA decay, with concomitant formation

Matthijs Raaben1, Marian J A Groot Koerkamp, Peter J M Rottier

  • 1Virology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.

Cellular Microbiology
|May 11, 2007
PubMed

Insights

Mouse hepatitis virus (MHV) triggers a cellular stress response, shutting down host protein synthesis via mRNA decay. However, MHV replication is enhanced when this host shutoff is impaired.

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • Viruses, including coronaviruses, often inhibit host protein synthesis to favor their own gene expression.
  • Understanding the mechanisms of viral-induced translational shutoff is crucial for comprehending virus-host interactions.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying host translational shutoff induced by mouse hepatitis coronavirus (MHV).
  • To determine the impact of MHV-induced translational shutoff on viral replication.

Main Methods:

  • Genome-wide microarray analysis of MHV-infected mouse cells.
  • Analysis of mRNA expression patterns, mRNA decay, and eukaryotic translation initiation factor 2alpha phosphorylation.
  • Observation of stress granules and processing bodies.

Main Results:

  • MHV infection led to downregulation of host mRNAs, particularly those involved in protein translation, mimicking a cellular stress response.
  • This mRNA downregulation was replication-dependent and mediated by mRNA decay.
  • Increased phosphorylation of eukaryotic translation initiation factor 2alpha and the formation of stress granules and processing bodies were observed.
  • MHV replication was not hindered, but rather enhanced, in cells with impaired host translational shutoff.

Conclusions:

  • MHV replication induces host translational shutoff by activating an integrated stress response pathway.
  • The inhibition of host protein synthesis is not beneficial for MHV replication in vitro and may even be detrimental.

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