单纯疱疹病毒Ⅰ型ICP0蛋白的E3泛素连接酶活性在抑制宿主免疫反应中的作用
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摘要
单纯疱疹病毒Ⅰ型(herpes simplex virus type 1,HSV-1)编码的具有泛素连接酶(ubiquitin-ligase enzymes 3,E3)活性的ICP0(infected cell protein 0)蛋白是病毒由潜伏期进入裂解复制期的关键作用蛋白。作为E3泛素连接酶,ICP0能够直接降解多种细胞组分,阻碍细胞多种固有免疫和先天性免疫反应。本文综述了ICP0的E3泛素连接活性在对抗宿主免疫反应中的作用。重点阐述了ICP0在裂解性复制中靶向降解宿主SUMO(small ubiquitin-like modifier)化修饰的抗病毒蛋白、阻碍宿主干扰素抗病毒途径和DNA损伤反应的相关机制。
E3 ubiquitin ligase infected cell protein 0(ICP0), encoded by herpes simplex virus type 1(HSV-1),regulates the switch between the lytic and latent states of HSV-1. As an E3 ubiquitin ligase, ICP0 directs the degradation of several cellular targets, allowing the virus counteract different cellular intrinsic and innate immune responses. In this review, we focus on how ICP0's E3 ubiquitin ligsase inactivates the host defenses to help the virus to survive. We put emphasis on the mechanisms of ICP0 in targeting degradation of the antiviral protein modified by SUMOs modified antiviral proteins, blocking host interferon antiviral pathway and DNA damage response.
E3 ubiquitin ligase infected cell protein 0(ICP0), encoded by herpes simplex virus type 1(HSV-1),regulates the switch between the lytic and latent states of HSV-1. As an E3 ubiquitin ligase, ICP0 directs the degradation of several cellular targets, allowing the virus counteract different cellular intrinsic and innate immune responses. In this review, we focus on how ICP0's E3 ubiquitin ligsase inactivates the host defenses to help the virus to survive. We put emphasis on the mechanisms of ICP0 in targeting degradation of the antiviral protein modified by SUMOs modified antiviral proteins, blocking host interferon antiviral pathway and DNA damage response.
引文
[1]Sacks WR,Schaffer PA.Deletion mutants in the gene encoding the herpes simplex virus type 1 immediate-early protein ICPO exhibit impaired growth in cell culture[J].JVirol,1987,61(3):829-839.
[2]Everett RD,Boutell C,Pheasant K,et al.Sequences related to SUMO interaction motifs in herpes simplex virus 1protein ICP0 act cooperatively to stimulate virus infection[J].J Virol,2014,88(5):2763-2774.
[3]Lanfranca MP,Mostafa HH,Davido DJ.HSV-1 ICP0:An E3 ubiquitin ligase that counteracts host intrinsic and innate immunity[J].Cells,2014,3(2):438-454.
[4]Vanni E,Gatherer D,Tong L,et al.Functional characterization of residues required for the herpes simplex virus 1 E3 ubiquitin ligase ICP0 to interact with the cellular E2 ubiquitin-conjugating enzyme UBE2D1(UbcH5a)[J].J Virol,2012,86(11):6323-6333.
[5]Boutell C,Sadis S,Everett RD.Herpes simplex virus type1 immediate-early protein ICP0 and is isolated RINGfinger domain act as ubiquitin E3 ligases in vitro[J].J Virol,2002,76(2):841-850.
[6]Canning M,Boutell C,Parkinson J,et al.A RING finger ubiquitin ligase is protected from autocatalyzed ubiquitination and degradation by binding to ubiquitinspecific protease USP7[J].J Bio Chem,2004,279(37):38160-38168.
[7]Boutell C,Cuchet Lourenco D,Vanni E,et al.A viral ubiquitin ligase has substrate preferential SUMO targeted ubiquitin ligase activity that counteracts intrinsic antiviral defence[J].PLoS Pathog,2011,7(9):e1002245.
[8]Sun H,Leverson JD,Hunter T.Conserved function of RNF4 family proteins in eukaryotes:targeting a ubiquitin ligase to SUMOylated proteins[J].EMBO J,2007,26(18):4102-4112.
[9]Gareau JR,Lima CD.The SUMO pathway:emerging mechanisms that shape specificity,conjugation and recognition[J].Nat Rev Mol Cell Biol,2010,11(12):861-871.
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[11]Hecker C,Rabiller M,Haglund K,et al.Specification of SUMO1-and SUMO2-interacting Motifs[J].J Bio Chem,2006,281(23):16117-16127.
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[14]Everett RD,Murray J.ND10 components relocate to sites associated with herpes simplex virus type 1 nucleoprotein complexes during virus infection[J].J Virol,2005.79(8):5078-5089.
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[16]Bernardi R,Papa A,Pandolfi PP.Regulation of apoptosis by PML and the PML-NBs[J].J Interferon Cytokine Res,2011,31(1):145-158.
[17]Cuchet Lourenco D,Boutell C,Lukashchuk V,et al.SUMOpathway dependent recruitment of cellular repressors to herpes simplex virus type 1 genomes[J].PLoS Pathog,2011,7(7):e1002123.
[18]Conn KL,Wasson P,Mcfarlane S,et al.Novel role for protein inhibitor of activated STAT 4(PIAS4)in the restriction of herpes simplex virus 1 by the cellular intrinsic antiviral immune response[J].J Virol,2016,90(9):4807-4826.
[19]Sahin U,Ferhi O,Carnec X,et al.Interferon controls SUMO availability via the Lin28 and let-7 axis to impede virus replication[J].Nat Commun,2014,5:4187.
[20]Muller S,Dejean A.Viral immediate-early proteins abrogate the modification by SUMO-1 of PML and Sp100proteins,correlating with nuclear body disruption[J].JVirol,1999,73(6):5137-5143.
[21]Sloan E,Tatham MH,Groslambert M,et al.Analysis of the SUMO2 proteome during HSV-1 infection[J].PLoS Pathog,2015,11(7):e1005059.
[22]Lukashchuk V,Everett RD.Regulation of ICP0-null mutant herpes simplex virus type 1 infection by ND10components ATRX and hDaxx[J].J Virol,2010,84(8):4026-4040.
[23]Brown JR,Conn KL,Wasson P,et al.SUMO ligase protein inhibitor of activated STAT1(PIAS1)is a constituent promyelocytic leukemia nuclear body protein that contributes to the intrinsic antiviral immune response to herpes simplex virus 1[J].J Virol,2016,90(13):5939-5952.
[24]Orzalli MH,Deluca NA,Knipe DM.Nuclear IFI16induction of IRF-3 signaling during herpesviral infection and degradation of IFI16 by the viral ICP0 protein[J].Proc Natl Acad Sci USA,2012,109(44):E3008-E3017.
[25]van Lint AL,Murawski MR,Goodbody RE,et al.Herpes simplex virus immediate-early ICP0 protein inhibits tolllike receptor 2-dependent inflammatory responses and NF-κB signaling[J].J Virol,2010,84(20):10802-10811.
[26]Lin R,Noyce RS,Collins SE,et al.The herpes simplex virus ICP0 RING finger domain inhibits IRF3-and IRF7-mediated activation of interferon-stimulated genes[J].JVirol,2004,78(4):1675-1684.
[27]张曦,张洁琼,罗琳林,等.Irf3基因缺失导致角膜组织对HSV-1病毒易感性增强[J].免疫学杂志,2019,35(2):112-118.
[28]Melroe GT,Silva L,Schaffer PA,et al.Recruitment of activated IRF-3 and CBP/p300 to herpes simplex virus ICP0 nuclear foci:potential role in blocking IFN-beta induction[J].Virology,2007,360(2):305-321.548
[29]Dantzer F,Ame JC,Schreiber V,et al.Poly(ADP-ribose)polymerase-1 activation during DNA damage and repair[J].Methods Enzymol,2006,409:493-510.
[30]Haince JF,Mcdonald D,Rodrigue A,et al.PARP1-dependent kinetics of recruitment of MRE11 and NBS1proteins to multiple DNA damage sites[J].J Biol Chem.2008,283(2):1197-1208.
[31]Turnell AS,Grand RJ.DNA viruses and the cellular DNA-damage response[J].Biomolecules,2016,6(1):2.
[32]Li H,Baskaran R,Krisky DM,et al.Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth[J].Virology,2008,375(1):13-23.
[33]Lees Miller SP,Long MC,Kilvert MA,et al.Attenuation of DNA-dependent protein kinase activity and its catalytic subunit by the herpes simplex virus type 1 transactivator ICP0[J].J Virol,1996,70(11):7471-7477.
[34]Lilley CE,Chaurushiya MS,Boutell C,et al.A viral E3ligase targets RNF8 and RNF168 to control histone ubiquitination and DNA damage responses[J].J Virol,1996,70(11):7471-7477.
[35]Grady SL,Hwang J,Vastag L,et al.Herpes simplex virus 1infection activates Poly(ADP-Ribose)polymerase and triggers the degradation of Poly(ADP-Ribose)glycohydrolase[J].J Virol,2012,86(15):8259-8268.
[36]杨荷丹,蒋娟.单纯疱疹病毒感染的复发机制与治疗的研究进展[J].中国麻风皮肤病杂志,2018,34(11):694-697.
[37]樊建勇,赵阳,杨慧兰.单纯疱疹病毒的潜伏、复发感染与防治[J].中国医学文摘·皮肤科学,2017,34(1):9-17.
[2]Everett RD,Boutell C,Pheasant K,et al.Sequences related to SUMO interaction motifs in herpes simplex virus 1protein ICP0 act cooperatively to stimulate virus infection[J].J Virol,2014,88(5):2763-2774.
[3]Lanfranca MP,Mostafa HH,Davido DJ.HSV-1 ICP0:An E3 ubiquitin ligase that counteracts host intrinsic and innate immunity[J].Cells,2014,3(2):438-454.
[4]Vanni E,Gatherer D,Tong L,et al.Functional characterization of residues required for the herpes simplex virus 1 E3 ubiquitin ligase ICP0 to interact with the cellular E2 ubiquitin-conjugating enzyme UBE2D1(UbcH5a)[J].J Virol,2012,86(11):6323-6333.
[5]Boutell C,Sadis S,Everett RD.Herpes simplex virus type1 immediate-early protein ICP0 and is isolated RINGfinger domain act as ubiquitin E3 ligases in vitro[J].J Virol,2002,76(2):841-850.
[6]Canning M,Boutell C,Parkinson J,et al.A RING finger ubiquitin ligase is protected from autocatalyzed ubiquitination and degradation by binding to ubiquitinspecific protease USP7[J].J Bio Chem,2004,279(37):38160-38168.
[7]Boutell C,Cuchet Lourenco D,Vanni E,et al.A viral ubiquitin ligase has substrate preferential SUMO targeted ubiquitin ligase activity that counteracts intrinsic antiviral defence[J].PLoS Pathog,2011,7(9):e1002245.
[8]Sun H,Leverson JD,Hunter T.Conserved function of RNF4 family proteins in eukaryotes:targeting a ubiquitin ligase to SUMOylated proteins[J].EMBO J,2007,26(18):4102-4112.
[9]Gareau JR,Lima CD.The SUMO pathway:emerging mechanisms that shape specificity,conjugation and recognition[J].Nat Rev Mol Cell Biol,2010,11(12):861-871.
[10]Hendriks IA,Vertegaal AC.A high-yield doublepurification proteomics strategy for the identification of SUMO sites[J].Nat Protoc,2016,11(9):1630-1649.
[11]Hecker C,Rabiller M,Haglund K,et al.Specification of SUMO1-and SUMO2-interacting Motifs[J].J Bio Chem,2006,281(23):16117-16127.
[12]Tavalai N,Stamminger T.New insights into the role of the subnuclear structure ND10 for viral infection[J].Biochim Biophy Acta,2008,1783(11):2207-2221.
[13]Glass M,Everett RD.Components of promyelocytic leukemia nuclear bodies(ND10)act cooperatively to repress herpesvirus infection[J].J Virol,2013,87(4):2174-2185.
[14]Everett RD,Murray J.ND10 components relocate to sites associated with herpes simplex virus type 1 nucleoprotein complexes during virus infection[J].J Virol,2005.79(8):5078-5089.
[15]Lilley CE,Chaurushiya MS,Boutell C,et al.The intrinsic antiviral defense to incoming HSV-1 genomes includes specific DNA repair proteins and is counteracted by the viral protein ICP0[J].PLoS Pathog,2011,7(6):e1002084.
[16]Bernardi R,Papa A,Pandolfi PP.Regulation of apoptosis by PML and the PML-NBs[J].J Interferon Cytokine Res,2011,31(1):145-158.
[17]Cuchet Lourenco D,Boutell C,Lukashchuk V,et al.SUMOpathway dependent recruitment of cellular repressors to herpes simplex virus type 1 genomes[J].PLoS Pathog,2011,7(7):e1002123.
[18]Conn KL,Wasson P,Mcfarlane S,et al.Novel role for protein inhibitor of activated STAT 4(PIAS4)in the restriction of herpes simplex virus 1 by the cellular intrinsic antiviral immune response[J].J Virol,2016,90(9):4807-4826.
[19]Sahin U,Ferhi O,Carnec X,et al.Interferon controls SUMO availability via the Lin28 and let-7 axis to impede virus replication[J].Nat Commun,2014,5:4187.
[20]Muller S,Dejean A.Viral immediate-early proteins abrogate the modification by SUMO-1 of PML and Sp100proteins,correlating with nuclear body disruption[J].JVirol,1999,73(6):5137-5143.
[21]Sloan E,Tatham MH,Groslambert M,et al.Analysis of the SUMO2 proteome during HSV-1 infection[J].PLoS Pathog,2015,11(7):e1005059.
[22]Lukashchuk V,Everett RD.Regulation of ICP0-null mutant herpes simplex virus type 1 infection by ND10components ATRX and hDaxx[J].J Virol,2010,84(8):4026-4040.
[23]Brown JR,Conn KL,Wasson P,et al.SUMO ligase protein inhibitor of activated STAT1(PIAS1)is a constituent promyelocytic leukemia nuclear body protein that contributes to the intrinsic antiviral immune response to herpes simplex virus 1[J].J Virol,2016,90(13):5939-5952.
[24]Orzalli MH,Deluca NA,Knipe DM.Nuclear IFI16induction of IRF-3 signaling during herpesviral infection and degradation of IFI16 by the viral ICP0 protein[J].Proc Natl Acad Sci USA,2012,109(44):E3008-E3017.
[25]van Lint AL,Murawski MR,Goodbody RE,et al.Herpes simplex virus immediate-early ICP0 protein inhibits tolllike receptor 2-dependent inflammatory responses and NF-κB signaling[J].J Virol,2010,84(20):10802-10811.
[26]Lin R,Noyce RS,Collins SE,et al.The herpes simplex virus ICP0 RING finger domain inhibits IRF3-and IRF7-mediated activation of interferon-stimulated genes[J].JVirol,2004,78(4):1675-1684.
[27]张曦,张洁琼,罗琳林,等.Irf3基因缺失导致角膜组织对HSV-1病毒易感性增强[J].免疫学杂志,2019,35(2):112-118.
[28]Melroe GT,Silva L,Schaffer PA,et al.Recruitment of activated IRF-3 and CBP/p300 to herpes simplex virus ICP0 nuclear foci:potential role in blocking IFN-beta induction[J].Virology,2007,360(2):305-321.548
[29]Dantzer F,Ame JC,Schreiber V,et al.Poly(ADP-ribose)polymerase-1 activation during DNA damage and repair[J].Methods Enzymol,2006,409:493-510.
[30]Haince JF,Mcdonald D,Rodrigue A,et al.PARP1-dependent kinetics of recruitment of MRE11 and NBS1proteins to multiple DNA damage sites[J].J Biol Chem.2008,283(2):1197-1208.
[31]Turnell AS,Grand RJ.DNA viruses and the cellular DNA-damage response[J].Biomolecules,2016,6(1):2.
[32]Li H,Baskaran R,Krisky DM,et al.Chk2 is required for HSV-1 ICP0-mediated G2/M arrest and enhancement of virus growth[J].Virology,2008,375(1):13-23.
[33]Lees Miller SP,Long MC,Kilvert MA,et al.Attenuation of DNA-dependent protein kinase activity and its catalytic subunit by the herpes simplex virus type 1 transactivator ICP0[J].J Virol,1996,70(11):7471-7477.
[34]Lilley CE,Chaurushiya MS,Boutell C,et al.A viral E3ligase targets RNF8 and RNF168 to control histone ubiquitination and DNA damage responses[J].J Virol,1996,70(11):7471-7477.
[35]Grady SL,Hwang J,Vastag L,et al.Herpes simplex virus 1infection activates Poly(ADP-Ribose)polymerase and triggers the degradation of Poly(ADP-Ribose)glycohydrolase[J].J Virol,2012,86(15):8259-8268.
[36]杨荷丹,蒋娟.单纯疱疹病毒感染的复发机制与治疗的研究进展[J].中国麻风皮肤病杂志,2018,34(11):694-697.
[37]樊建勇,赵阳,杨慧兰.单纯疱疹病毒的潜伏、复发感染与防治[J].中国医学文摘·皮肤科学,2017,34(1):9-17.