Interferon-induced inhibiton of parainfluenza virus type 5; the role of MxA, PKR and oligo A synthetase/RNase L.

T S Carlos, D Young, S Stertz, G Kochs, Richard Edward Randall

Research output: Contribution to journalArticlepeer-review

Abstract

We have previously reported that the addition of interferon (IFN) to the culture medium of Vero cells (which cannot produce IFN) that were infected with the CPI- strain of parainfluenza virus 5 (PIV5, formally known as SV5), that fails to block IFN signaling, rapidly induces alterations in the relative levels of virus mRNA and protein synthesis. In addition, IFN treatment also caused a rapid redistribution of virus proteins and enhanced the formation of cytoplasmic viral inclusion bodies. The most studied IFN-induced genes with known anti-viral activity are MxA, PKR and the Oligo A synthetase/RNase L system. We therefore examined the effects of these proteins on the replication cycle of PIV5. These studies revealed that while these proteins had some anti-viral activity against PIV5 they were not primarily responsible for the very rapid alteration in virus protein synthesis observed following IFN treatment, nor for the IFN-induced formation of virus inclusion bodies, in CPI- infected cells. (C) 2007 Elsevier Inc. All rights reserved.

Original languageEnglish
Pages (from-to)166-173
Number of pages8
JournalVirology
Volume363
DOIs
Publication statusPublished - 20 Jun 2007

Keywords

  • parainflueza virus type 5
  • interferon
  • PKR
  • OAS
  • MxA
  • DEPENDENT PROTEIN-KINASE
  • PARA-INFLUENZA VIRUS
  • TRANSGENIC MICE
  • CROSSE VIRUS
  • NS1 PROTEIN
  • V-PROTEINS
  • CELLS
  • SIMIAN-VIRUS-5
  • CANINE
  • REPLICATION

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