Knockout of the Host Resistance Gene Pkr Fully Restores Replication of Murine Cytomegalovirus m142 and m143 Mutants In Vivo

J Virol. 2015 Oct 28;90(2):1144-7. doi: 10.1128/JVI.02003-15. Print 2016 Jan 15.

Abstract

Murine cytomegalovirus (MCMV) proteins m142 and m143 are essential for viral replication. They bind double-stranded RNA and prevent protein kinase R-induced protein synthesis shutoff. Whether the two viral proteins have additional functions such as their homologs in human cytomegalovirus do remained unknown. We show that MCMV m142 and m143 knockout mutants attain organ titers equivalent to those attained by wild-type MCMV in Pkr knockout mice, suggesting that these viral proteins do not encode additional PKR-independent functions relevant for pathogenesis in vivo.

MeSH terms

  • Animals
  • Mice, Knockout
  • Muromegalovirus / genetics
  • Muromegalovirus / physiology*
  • Mutation*
  • Viral Load
  • Viral Proteins / genetics*
  • Virus Replication*
  • eIF-2 Kinase / deficiency*

Substances

  • Viral Proteins
  • eIF-2 Kinase
  • protein kinase R, mouse

Grants and funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.