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

被引:13
作者
Carlos, T. S.
Young, D.
Stertz, S.
Kochs, G.
Randall, R. E. [1 ]
机构
[1] Univ St Andrews, Sch Biol, St Andrews KY16 9ST, Fife, Scotland
[2] Univ Freiburg, Dept Virol, D-79104 Freiburg, Germany
基金
英国惠康基金;
关键词
parainflueza virus type 5; interferon; PKR; OAS; MxA;
D O I
10.1016/j.virol.2007.01.014
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:166 / 173
页数:8
相关论文
共 37 条
[1]   Characterization of transgenic mice with targeted disruption of the catalytic domain of the double-stranded RNA-dependent protein kinase, PKR [J].
Abraham, N ;
Stojdl, DF ;
Duncan, PI ;
Méthot, N ;
Ishii, T ;
Dubé, M ;
Vanderhyden, BC ;
Atkins, HL ;
Gray, DA ;
McBurney, MW ;
Koromilas, AE ;
Brown, EG ;
Sonenberg, N ;
Bell, JC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (09) :5953-5962
[2]   The V proteins of paramyxoviruses bind the IFN-inducible RNA helicase, mda-5, and inhibit its activation of the IFN-β promoter [J].
Andrejeva, J ;
Childs, KS ;
Young, DF ;
Carlos, TS ;
Stock, N ;
Goodbourn, S ;
Randall, RE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (49) :17264-17269
[3]   Degradation of STAT1 and STAT2 by the V proteins of simian virus 5 and human parainfluenza virus type 2, respectively: Consequences for virus replication in the presence of alpha/beta and gamma interferons [J].
Andrejeva, J ;
Young, DF ;
Goodbourn, S ;
Randall, RE .
JOURNAL OF VIROLOGY, 2002, 76 (05) :2159-2167
[4]  
Arnheiter H, 1996, CURR TOP MICROBIOL, V206, P119
[5]   PERSISTENT INFECTION OF VERO CELLS BY PARAMYXOVIRUSES - A MORPHOLOGICAL AND IMMUNOELECTRON MICROSCOPIC INVESTIGATION [J].
BAUMGARTNER, W ;
KRAKOWKA, S ;
BLAKESLEE, JR .
INTERVIROLOGY, 1987, 27 (04) :218-223
[6]  
BAUMGARTNER WK, 1982, VET PATHOL, V19, P79, DOI 10.1177/030098588201900111
[7]   REVERSAL OF THE INTERFERON-SENSITIVE PHENOTYPE OF A VACCINIA VIRUS LACKING E3L BY EXPRESSION OF THE REOVIRUS S4 GENE [J].
BEATTIE, E ;
DENZLER, KL ;
TARTAGLIA, J ;
PERKUS, ME ;
PAOLETTI, E ;
JACOBS, BL .
JOURNAL OF VIROLOGY, 1995, 69 (01) :499-505
[8]   Interferon-induced alterations in the pattern of parainfluenza virus 5 transcription and protein synthesis and the induction of virus inclusion bodies [J].
Carlos, TS ;
Fearns, R ;
Randall, RE .
JOURNAL OF VIROLOGY, 2005, 79 (22) :14112-14121
[9]   Relationships and host range of human, canine, simian and porcine isolates of simian virus 5 (parainfluenza virus 5) [J].
Chatziandreou, N ;
Stock, N ;
Young, D ;
Andrejeva, J ;
Hagmaier, K ;
McGeoch, DJ ;
Randall, RE .
JOURNAL OF GENERAL VIROLOGY, 2004, 85 :3007-3016
[10]   Differences in interferon sensitivity and biological properties of two related isolates of simian virus 5: A model for virus persistence [J].
Chatziandreou, N ;
Young, D ;
Andrejeva, J ;
Goodbourn, S ;
Randall, RE .
VIROLOGY, 2002, 293 (02) :234-242