Li Kui
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, USA.
Methods Mol Biol. 2009;510:211-26. doi: 10.1007/978-1-59745-394-3_16.
Interferon regulatory factor 3 (IRF-3) is a ubiquitously expressed latent cellular transcription factor that plays a pivotal role in control of innate, type I interferon (IFN) antiviral responses. After viral infections, IRF-3 is activated by specific C-terminal phosphorylation, which induces its dimerization and nuclear translocation, whereupon IRF-3 activates the transcription of type I IFNs and a number of other antiviral effector genes. Many viruses have evolved strategies that antagonize signaling mechanisms leading to IRF-3 activation. Recent studies have shown that hepatitis C virus blocks IRF-3 activation and subsequent IFN induction by cleaving critical cellular substrates within the intracellular antiviral signaling pathways upstream of IRF-3 with its major protease, NS3/4A.
干扰素调节因子3（IRF-3）是一种广泛表达的潜伏性细胞转录因子，在先天性I型干扰素（IFN）抗病毒反应的控制中起关键作用。病毒感染后，IRF-3通过特定的C端磷酸化被激活，这诱导其二聚化和核转位，随后IRF-3激活I型IFN和许多其他抗病毒效应基因的转录。许多病毒已经进化出对抗导致IRF-3激活的信号机制的策略。最近的研究表明，丙型肝炎病毒通过用其主要蛋白酶NS3/4A切割IRF-3上游细胞内抗病毒信号通路中的关键细胞底物，阻断IRF-3激活及随后的IFN诱导。
