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Hepatitis B virus X protein suppresses virus-triggered IRF3 activation and IFN-β induction by disrupting the VISA-associated complex

肝炎 B 病毒 X 蛋白质由破坏联系维萨卡的建筑群压制被触发病毒的 IRF3 激活和 IFN- 尾正式就职

作     者:Xianmiao Wang Ying Li Aiping Mao Chao Li Yongkui Li Po Tien 

作者机构:College of Life SciencesModern Virology CenterWuhan UniversityWuhan 430072China 

出 版 物:《Cellular & Molecular Immunology》 (中国免疫学杂志(英文版))

年 卷 期:2010年第7卷第5期

页      面:341-348页

核心收录:

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基  金:supported by grants from the 973 Program of China(No.2006CB504301) 

主  题:HBx innate immunity signal transduction type I interferons VISA 

摘      要:Viral RNAs produced during viral infection are recognized by the cytoplasmic RNA helicases retinoic acid-inducible gene-I(RIG-I)and melanoma differentiation-associated gene 5(MDA5).A central adapter protein downstream of RIG-I and MDA5 is the mitochondrial membrane protein virus-induced signaling adaptor(VISA),which mediates the induction of type I interferons(IFNs)through the activation of transcription factors such as nuclear factor-kappaB(NF-kB)and IFN-regulatory factor-3(IRF3).Here we found that hepatitis B virus(HBV)-encoded X protein(HBx)acts as an inhibitor of virus-triggered IRF3 activation and IFN-b *** and plaque assays indicate that HBx inhibits signaling by components upstream but not downstream of *** experiments indicate that HBx interacts with VISA and disrupts the association of VISA with its upstream and downstream *** findings suggest that HBx acts as a suppressor of virus-triggered induction of type I IFNs,which explains the observation that HBV causes transient and chronic infection in hepatocytes but fails to activate the pattern recognition receptor-mediated IFN induction pathways.

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