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The cellular protein P58IPK regulates influenza virus mRNA translation and replication through a PKR-mediated

Alan G Goodman1, Jennifer A Smith, Siddharth Balachandran

  • 1Department of Microbiology, University of Washington, Box 358070, Seattle, WA 98195-8070, USA.

Journal of Virology
|December 15, 2006
PubMed

Insights

P58(IPK) is crucial for efficient influenza virus mRNA translation by inhibiting PKR, a key kinase. Its absence impairs viral translation, while its target PKR

Area of Science:

  • Molecular Biology
  • Virology
  • Immunology

Background:

  • P58(IPK) inhibits PKR and PERK, kinases targeting eIF2alpha.
  • This suggests P58(IPK) regulates cellular and viral mRNA translation.
  • Its precise role in viral infection requires definition.

Purpose of the Study:

  • To define the role of P58(IPK) in mammalian cell viral infections.
  • To investigate the mechanism of P58(IPK) in regulating influenza virus mRNA translation.

Main Methods:

  • Utilized P58(IPK-/-) mouse embryo fibroblasts.
  • Examined viral replication and mRNA translation in knockout and wild-type cells.
  • Investigated the role of PKR and PERK in P58(IPK) function.

Main Results:

  • Absence of P58(IPK) increased eIF2alpha phosphorylation and decreased influenza virus translation.
  • P58(IPK-/-) cells showed reduced VSV replication but enhanced reovirus yields.
  • Reversed trends were observed in PKR-deficient cells, indicating PKR's role.
  • PERK absence had minimal impact on influenza virus translation.

Conclusions:

  • P58(IPK) regulates influenza virus mRNA translation and infection via a PKR-dependent pathway.
  • This mechanism is independent of PERK.
  • P58(IPK) is a critical host factor for efficient influenza virus replication.

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