小鼠肝炎病毒不会诱导β干扰素的合成，也不会抑制双链RNA对其的诱导作用。
Mouse hepatitis virus does not induce Beta interferon synthesis and does not inhibit its induction by double-stranded RNA.
作者信息
Zhou Haixia, Perlman Stanley
机构信息
Department of Microbiology, University of Iowa, Bowen Science Building 3-730, Iowa City, IA 52242, USA.
出版信息
J Virol. 2007 Jan;81(2):568-74. doi: 10.1128/JVI.01512-06. Epub 2006 Nov 1.
Abstract
Mouse hepatitis virus (MHV) does not induce interferon (IFN) production in fibroblasts or bone marrow-derived dendritic cells. In this report, we show that the essential IFN-beta transcription factors NF-kappaB and IFN regulatory factor 3 are not activated for nuclear translocation and gene induction during infection. However, MHV was unable to inhibit the activation of these factors and subsequent IFN-beta production induced by poly(I:C). Further, MHV infection did not inhibit IFN-beta production mediated by known host pattern recognition receptors (PRRs) (RIG-I, Mda-5, and TLR3). These results are consistent with the notion that double-stranded RNA, produced during MHV infection, is not accessible to cellular PRRs.
摘要
小鼠肝炎病毒（MHV）不会在成纤维细胞或骨髓来源的树突状细胞中诱导干扰素（IFN）产生。在本报告中，我们表明，在感染期间，关键的IFN-β转录因子NF-κB和IFN调节因子3不会被激活以进行核转位和基因诱导。然而，MHV无法抑制这些因子的激活以及由聚肌苷酸胞苷酸（poly(I:C)）诱导的后续IFN-β产生。此外，MHV感染不会抑制由已知宿主模式识别受体（PRR）（视黄酸诱导基因I（RIG-I）、黑色素瘤分化相关基因5（Mda-5）和Toll样受体3（TLR3））介导的IFN-β产生。这些结果与以下观点一致，即在MHV感染期间产生的双链RNA无法被细胞PRR识别。
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