Group 2 coronaviruses prevent immediate early interferon induction by protection of viral RNA from host cell recognition

被引：104

作者：

Versteeg, Gijs A. ^{[1
]}

Bredenbeek, Peter J. ^{[1
]}

van den Worm, Sjoerd H. E. ^{[1
]}

Spaan, Willy J. M. ^{[1
]}

机构：

[1] Leiden Univ, Med Ctr, Mol Virol Lab, Dept Med Microbiol,Ctr Infect Dis, NL-2300 RC Leiden, Netherlands

来源：

VIROLOGY | 2007年 / 361卷 / 01期

关键词：

coronavirus; murine hepatitis virus; MHV; SARS; SARS-CoV; interferon; IFN; antagonist; poly (I : C); Sendai virus;

D O I：

10.1016/j.virol.2007.01.020

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Many viruses encode antagonists to prevent interferon (IFN) induction. Infection of fibroblasts with the murine hepatitis coronavirus (MHV) and SARS-coronavirus (SARS-CoV) did not result in nuclear translocation of interferon-regulatory factor 3 (IRF3), a key transcription factor involved in IFN induction, and induction of IFN mRNA transcription. Furthermore, MHV and SARS-CoV infection could not prevent IFN induction by poly (I:C) or Sendai virus, suggesting that these CoVs do not inactivate IRF3-mediated transcription regulation, but apparently prevent detection of replicative RNA by cellular sensory molecules. Our data indicate that shielding of viral RNA to host cell sensors might be the main general mechanism for coronaviruses to prevent IFN induction. (c) 2007 Elsevier Inc. All rights reserved.

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收藏

页码：18 / 26

页数：9

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