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Journal of Virology, November 2005, p. 14112-14121, Vol. 79, No. 22
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.22.14112-14121.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Interferon-Induced Alterations in the Pattern of Parainfluenza Virus 5 Transcription and Protein Synthesis and the Induction of Virus Inclusion Bodies

T. S. Carlos,1 R. Fearns,2 and R. E. Randall1*

School of Biology, University of St. Andrews, Fife KY16 9TS, Scotland, United Kingdom,1 Molecular and Cellular Pathology, Division of Pathology and Neuroscience, University of Dundee, Dundee DD1 9SY, Scotland, UK2

Received 27 June 2005/ Accepted 18 August 2005

Although parainfluenza virus 5 (simian virus 5 [SV5]) circumvents the interferon (IFN) response by blocking IFN signaling and by reducing the amount of IFN released by infected cells, its ability to circumvent the IFN response is not absolute. The effects of IFN on SV5 infection were examined in Vero cells, which do not produce but can respond to IFN, using a strain of SV5 (CPI–) which does not block IFN signaling. Thus, by infecting Vero cells with CPI– and subsequently treating the cells with exogenous IFN, it was possible to observe the effects that IFN had on SV5 infection in the absence of virus countermeasures. IFN rapidly (within 6 h) induced alterations in the relative levels of virus mRNA and protein synthesis and caused a redistribution of virus proteins within infected cells that led to the enhanced formation of virus cytoplasmic inclusion bodies. IFN induced a steeper gradient of mRNA transcription from the 3' to the 5' end of the genome and the production of virus mRNAs with longer poly(A) tails, suggesting that the processivity of the virus polymerase was altered in cells in an IFN-induced antiviral state. Additional evidence is presented which suggests that these findings also apply to the replication of strains of SV5, parainfluenza virus type 2, and mumps virus that block IFN signaling when they infect cells that are already in an IFN-induced antiviral state.

* Corresponding author. Mailing address: School of Biology, University of St. Andrews, Fife KY16 9TS, Scotland, United Kingdom. Phone: 44 1334 463397. Fax: 44 1334 462595. E-mail: rer{at}st-and.ac.uk.

Journal of Virology, November 2005, p. 14112-14121, Vol. 79, No. 22
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.22.14112-14121.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Randall, R. E., Goodbourn, S. (2008). Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. J. Gen. Virol. 89: 1-47 [Abstract] [Full Text]  
  • Hale, B. G., Jackson, D., Chen, Y.-H., Lamb, R. A., Randall, R. E. (2006). Influenza A virus NS1 protein binds p85beta and activates phosphatidylinositol-3-kinase signaling. Proc. Natl. Acad. Sci. USA 103: 14194-14199 [Abstract] [Full Text]  


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