Hepatitis B virus hijacks CTHRC1 to evade host immunity and maintain replication

查看全文 作　　者：Lan [1]Bai;Wei [1]Zhang;Li [1]Tan;Hongchuan [1]Yang;Maolin [1]Ge;Chengliang [1]Zhu;Rui [1]Zhang;Yanhua [1]Cao;Junbo [1]Chen;Zhen [1]Luo;Wenzhe [1]Ho;Fang [1]Liu;Kailang [1]Wu;Jianguo [1]Wu

机构地区：[1]State Key Laboratory of Virology and College of Life Sciences,Wuhan University,Wuhan 430072,China

出　　处：《Journal of Molecular Cell Biology》索引2015年第7卷第6期,共14页

基　　金：supported by research grants from theMajor State Basic ResearchDevelopment Program(973 Program)(grant number 2012CB518900);the National Natural Science Foundation of China(grant numbers 31230005,31270206,31200134,and 81171525);the National Mega Project on Major Infectious Disease Prevention(grant numbers 2012ZX10002006-003 and 2012ZX10004-207);the Chinese Foundation for Hepatitis Prevention and Control(grant number CFHPC20132153). 摘　　要：HepatitisBvirus(HBV)infection causes acuteand chronic liver diseases,but is not directly cytopathic.Liver injury results fromrepeated attempts of the cellular immune response system to control the viral infection.Here,we investigate the roles of cellular factors and signaling pathways involved in the regulation of HBV replication to reveal the mechanism underlying HBV infection and pathogenesis.Weshowthat collagen triple helix repeat containing 1(CTHRC1)expression is elevated in HBV-infected patients andin HBV-transfected cells through epigenetic modification and transcriptional regulation.CTHRC1 facilitates HBV replication in cultured cells and BALB/c mice by activating the PKCa/ERK/JNK/c-Jun cascade to repress the IFN/JAK/STAT pathway.HBV-activated CTHRC1 downregulates the activityof typeI interferon(IFN),theproductionof IFN-stimulatedgenes(ISGs),andthephosphorylationofsignal transducerandactivator of transcription 1/2(STAT1/2),whereas it upregulates the phosphorylation and ubiquitination of type I IFN receptors(IFNARa/b).Thus,our results showthat HBV uses a novelmechanismto hijack cellular factors and signal cascades in order to evade host antiviral immunity and maintain persistent infection.We also demonstrate that CTHRC1 has a novel role in viral infection. 关键词：hepatitis B virus collagen triple helix repeat containing 1(CTHRC1) immune response immune evasion PKC/JNK/ERK/c-Jun cascade IFN/JAK/STAT pathway

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Hepatitis B virus hijacks CTHRC1 to evade host immunity and maintain replication

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