Versteeg Gijs A, Bredenbeek Peter J, van den Worm Sjoerd H E, Spaan Willy J M
Molecular Virology Laboratory, Department of Medical Microbiology, Center of Infectious Diseases, Leiden University Medical Center, LUMC E4-P, P.O. Box 9600, 2300 RC Leiden, The Netherlands.
Virology. 2007 Apr 25;361(1):18-26. doi: 10.1016/j.virol.2007.01.020. Epub 2007 Feb 21.
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.
许多病毒编码拮抗剂以阻止干扰素(IFN)的诱导。用鼠肝炎冠状病毒(MHV)和严重急性呼吸综合征冠状病毒(SARS-CoV)感染成纤维细胞,不会导致参与IFN诱导的关键转录因子干扰素调节因子3(IRF3)的核转位,也不会诱导IFN mRNA转录。此外,MHV和SARS-CoV感染不能阻止聚肌胞苷酸(poly(I:C))或仙台病毒诱导的IFN,这表明这些冠状病毒不会使IRF3介导的转录调节失活,而是显然阻止细胞传感分子检测复制性RNA。我们的数据表明,将病毒RNA与宿主细胞传感器屏蔽可能是冠状病毒阻止IFN诱导的主要普遍机制。