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

13 Citations (Scopus)

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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