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Protein synthesis shut-off induced by influenza virus infection is independent of PKR activity

T Zürcher1, R M Marión, J Ortín

  • 1Centro Nacional de Biotecnología (CSIC), Campus de Cantoblanco, 28049 Madrid, Spain.

Journal of Virology
|August 23, 2000
PubMed

Insights

Influenza virus infection does not rely on PKR activity or nuclear events for host cell shut-off. Viral mRNA accumulation correlates with cellular mRNA decay, regardless of NS1 protein mutations.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Influenza virus infection triggers host cell shut-off, a process impacting cellular functions.
  • The role of Protein Kinase R (PKR) and nuclear events in this shut-off mechanism remains incompletely understood.

Purpose of the Study:

  • To investigate the role of PKR activity in influenza virus-induced host cell shut-off.
  • To determine the relevance of inhibited pre-mRNA polyadenylation and nucleocytoplasmic transport in virus-induced shut-off.

Main Methods:

  • Infection of PKR-positive (PKR(+)) and PKR-negative (PKR(-)) cell cultures.
  • Metabolic labeling in vivo to assess protein synthesis.
  • Experiments using influenza viruses with mutations in the NS1 protein (lacking C-terminal sequences).
  • Analysis of cytoplasmic mRNA stability.

Main Results:

  • No significant differences in viral protein synthesis or cellular protein synthesis decay were observed between PKR(+) and PKR(-) cells.
  • Mutant influenza viruses lacking NS1 C-terminal sequences did not alter the shut-off phenotype compared to wild-type viruses.
  • Accumulation of viral mRNA during infection correlated with progressive decay of cellular mRNA in both wild-type and NS1 mutant infections.

Conclusions:

  • PKR activity is not essential for influenza virus-induced host cell shut-off.
  • Nuclear events like pre-mRNA polyadenylation and nucleocytoplasmic transport inhibition are not critical for this shut-off.
  • The decay of cellular mRNA in the cytoplasm is a key feature accompanying viral mRNA accumulation during influenza infection.

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