猫杯状病毒引起细胞凋亡的信号转导通路研究进展
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摘要
猫杯状病毒(Feline calicivirus,FCV)是猫科动物上呼吸系统疾病的常见病因,威胁野生猫科动物和家猫的健康。FCV在体外培养过程中会引起CRFK等细胞的凋亡,导致明显的细胞病变。近年来已有FCV对细胞凋亡转导通路影响的研究,其中较为详细的是线粒体转导通路,但对FCV影响细胞凋亡机制的研究尚不完整。本文对FCV结构特征及诱导凋亡产生的细胞病理变化和相关信号转导途径的现阶段研究情况展开综述,以期为FCV致病机制的深入研究和该病治疗方法的探索提供参考及理论依据。
The feline calicivirus(FCV)is a common cause of upper respiratory tract infection in felines,and threatens the health of wild and domestic felines. The FCV can cause apoptosis and significant cytopathic effects in many cell types,such as Crandell-Rees feline kidney cells. In recent years,scholars have investigated the effect of the FCV on apoptosis-related transduction pathways,focusing more on mitochondrial signal transduction. However,studies on how the FCV affects apoptosis are lacking. We reviewed the structural characteristics of the FCV,the effects of FCV-induced apoptosis on cytopathological changes,and how the FCV affected the related signal-transduction pathways. In this way,our review provides a reference and theoretical basis for indepth study of FCV pathogenesis and exploration of the corresponding treatment methods.
The feline calicivirus(FCV)is a common cause of upper respiratory tract infection in felines,and threatens the health of wild and domestic felines. The FCV can cause apoptosis and significant cytopathic effects in many cell types,such as Crandell-Rees feline kidney cells. In recent years,scholars have investigated the effect of the FCV on apoptosis-related transduction pathways,focusing more on mitochondrial signal transduction. However,studies on how the FCV affects apoptosis are lacking. We reviewed the structural characteristics of the FCV,the effects of FCV-induced apoptosis on cytopathological changes,and how the FCV affected the related signal-transduction pathways. In this way,our review provides a reference and theoretical basis for indepth study of FCV pathogenesis and exploration of the corresponding treatment methods.
引文
[1]Battilani M,Vaccari F,Carelle M S,Morandi F,Benazzi C,Kipar A,Dondi F,Scagliarini A.Virulent feline calicivirus disease in a shelter in Italy:A case description[J].Res Vet Sci,2013,95(1):283-290.
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[4]Cite images created with the PDB ID and associated publication,NGL Viewer(AS Roseet al.(2018)NGLviewer:web-based molecular graphics for large complexes.Bioinformatics dio:10.1093/bioinformatics/bty419),and RCSB PDB[EB/OL].http://www.rcsb.org/3dview/3M8L/1.
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[9]Lindsay J,Esposti M D,Gilmore A P.Bcl-2 proteins and mitochondria-specificity in membrane targeting for death.[J].BBA-Biomembranes,2011,1813(4):532-539.
[10]Willcocks M M,Carter M J,Roberts L O.Cleavage of eukaryotic initiation factor eIF4G and inhibition of hostcell protein synthesis during feline calicivirus infection[J].J Gen Virol,2004,85(Pt 5):1125-1130.
[11]Natoni A.The mitochondrial pathway of apoptosis is triggered during feline calicivirus infection[J].J Gen Virol,2006,87(2):357-361.
[12]Bok K,Prikhodko V G,Green K Y,Sosnovtsev S V.Apoptosis in murine norovirus-infected RAW264.7 cells is associated with downregulation of survivin[J].J Virol,2009,83(8):3647-3656.
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[18]Romero-Brey I,Bartenschlager R,Romero-Brey I,Bartenschlager R.Endoplasmic reticulum:the favorite intracellular niche for viral replication and assembly[J].Viruses,2016,8(6):160-160.
[19]Sharp T M,Guix S,Katayama K,Crawford S E,Estes M K.Inhibition of cellular protein secretion by norwalk virus nonstructural protein p22 requires a mimic of an endoplasmic reticulum export signal[J/OL].PLoSOne,2010,5(10):e13130.
[20]Urakova N,Frese M,Hall R N,Liu J,Matthaei M,Strive T.Expression and partial characterisation of rabbit haemorrhagic disease virus non-structural proteins[J].Virology,2015,484:69-79.
[21]udshoorn D,Hoeven B van der,Limpens R W A L,Beugeling C,Snijder E J,Bárcena M,Kikkert M.Antiviral innate immune response interferes with the formation of replication-associated membrane structures induced by a positive-strand RNA virus[J/OL].MBio,2016,7(6):e 01991-16.
[22]Wang M,Kaufman R J.Protein misfolding in the endoplasmic reticulum as a conduit to human disease[J].Nature,2016,529(7586):326-335.
[23]Hetz C,Papa F R.The unfolded protein response and cell fate control[J].Mol Cell,2018,69(2):169-181.
[24]Bailey D,Kaiser W J,Hollinshead M,Moffat K,Chaudhry Y,Wileman T,Sosnovtsev S V,Goodfellow I G.Feline calicivirus p32,p39 and p30 proteins localize to the endoplasmic reticulum to initiate replication complex formation[J].J Gen Virol,2010,91(3):739-749.
[25]Alvarez-Sanchez C,Cancio-Lonches C,Mora-Heredia JE,Santos-Valencia J C,Barrera-Vázquez O S,Yocupicio-Monroy M.Negative effect of heat shock on feline calicivirus release from infected cells is associated with the control of apoptosis[J].Virus Res,2015,198:44-52.
[26]Humoud M N,Doyle N,Royall E,Willcocks M M,Sorgeloos F,Kuppeveld F van,Roberts L O,Goodfellow I G,Langereis M A,Locker N.Feline Calicivirus infection disrupts the assembly of cytoplasmic stress granules and induces G3BP1 cleavage[J].J Virol,2016,90(14):6489-6501.
[27]Dickens L S,Powley I R,Hughes M A,MacFarlane M.The‘complexities’of life and death:Death receptor signalling platforms[J].Exp Cell Res,2012,318(11):1269-1277.
[28]Galluzzi L,Vitale I,Aaronson S A,et al.Molecular mechanisms of cell death:recommendations of the Nomenclature Committee on Cell Death 2018[J].Cell Death Differ,2018,25(3):486-541.
[29]Newton K,Dixit V M.Signaling in innate immunity and inflammation[J].Cold Spring Harb Perspect Bio,2012,4(3):a006049-a006049.
[30]Bousoik E,Montazeri Aliabadi H.“Do We Know Jack”about JAK?A closer look at JAK/STAT signaling pathway[J].Front Oncol,2018,8:287-287.
[31]刘永相.猫杯状病毒感染抑制Ⅰ型干扰素信号通路的分子机制[D].中国农业科学院,2018.
[32]Rongvaux A,Jackson R,Harman C C D,Li T,West A P,de Zoete M R,Wu Y,Yordy B,Lakhani S A,Kuan C-Y,Taniguchi T,Shadel G S,Chen Z J,Iwasaki A,Flavell R A.Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA[J].Cell,2014,159(7):1563-1577.
[33]Chattopadhyay S,Marques J T,Yamashita M,Peters K L,Smith K,Desai A,Williams B R G,Sen G C.Viral apoptosis is induced by IRF-3-mediated activation of Bax[J].EMBO J,2010,29(10):1762-1773.
[34]Yumiketa Y,Narita T,Inoue Y,Sato G,Kamitani W,Oka T,Katayama K,Sakaguchi T,Tohya Y.Nonstructural protein p39 of feline calicivirus suppresses host innate immune response by preventing IRF-3 activation[J].Vet Microbiol,2016,185:62-67.
[35]Jeong S I,Kim J W,Ko K P,Ryu B K,Lee M G,Kim H J,Chi S G.XAF1 forms a positive feedback loop with IRF-1 to drive apoptotic stress response and suppress tumorigenesis[J].Cell Death Dis,2018,9(8):806-806.
[36]Liu Y,Liu X,Kang H,Hu X,Liu J,Tian J,Qu L.Identification of feline interferon regulatory factor 1 as an efficient antiviral factor against the replication of feline calicivirus and other feline viruses[J].Biomed Res Int,2018,1-10.
[37]Alfajaro M M,Choi J S,Kim D S,Seo J Y,Kim J Y,Park J G,Soliman M,Baek Y B,Cho E H,Kwon J,Kwon H J,Park S J,Lee W S,Kang M I,Hosmillo M,Goodfellow I,Cho K O.Activation of COX-2/PGE2 promotes sapovirus replication via the inhibition of nitric oxide production[J].J Virol,2017,91(3):01656-01656.
[38]Alfajaro M M,Cho E H,Park J G,Kim J Y,Soliman M,Baek Y B,Kang M I,Park S I,Cho K O.Feline calicivirus-and murine norovirus-induced COX-2/PGE2signaling pathway has proviral effects[J/OL].PLoSOne,2018,13(7):e0200726.
[39]Akadera T,Yumoto H,Tozuka Y,Ohyashiki T.Prostaglandin E2 induces caspase-dependent apoptosis in rat cortical cells[J].Neurosci Lett,2002,317(2):61-64.
[2]August J R,BVetMed,MRCVS.Consultations in Feline Internal Medicine(Fifth Edition)[M].Consultations in Feline Internal Medicine 06.Elsevier LTD,Oxford,2009.
[3]Conley M J.Structural and functional characterisation of feline calicivirus entry[D].University of Glasgow,2018.
[4]Cite images created with the PDB ID and associated publication,NGL Viewer(AS Roseet al.(2018)NGLviewer:web-based molecular graphics for large complexes.Bioinformatics dio:10.1093/bioinformatics/bty419),and RCSB PDB[EB/OL].http://www.rcsb.org/3dview/3M8L/1.
[5]黄倩倩,刘家森,田进,孔德生,曲连东.猫杯状病毒的分离鉴定及其对理化因素抵抗力的研究[J].中国兽医科学,2015(4):385-389.
[6]Sosnovtsev S V,Prikhod’ko E A,Belliot G,Cohen JI,Green K Y.Feline calicivirus replication induces apoptosis in cultured cells[J].Virus Res,2003,94(1):1-10.
[7]Fischer U,J?nicke R U,Schulze-Osthoff K.Many cuts to ruin:a comprehensive update of caspase substrates.[J].Cell Death Differ,2003,10(1):76-100.
[8]Brenner D,Mak T W.Mitochondrial cell death effectors.[J].Curr Opin Cell Biol,2009,21(6):871-877.
[9]Lindsay J,Esposti M D,Gilmore A P.Bcl-2 proteins and mitochondria-specificity in membrane targeting for death.[J].BBA-Biomembranes,2011,1813(4):532-539.
[10]Willcocks M M,Carter M J,Roberts L O.Cleavage of eukaryotic initiation factor eIF4G and inhibition of hostcell protein synthesis during feline calicivirus infection[J].J Gen Virol,2004,85(Pt 5):1125-1130.
[11]Natoni A.The mitochondrial pathway of apoptosis is triggered during feline calicivirus infection[J].J Gen Virol,2006,87(2):357-361.
[12]Bok K,Prikhodko V G,Green K Y,Sosnovtsev S V.Apoptosis in murine norovirus-infected RAW264.7 cells is associated with downregulation of survivin[J].J Virol,2009,83(8):3647-3656.
[13]Roberts L O,Al-Molawi N,Carter M J,Kass G E N.Apoptosis in cultured cells infected with feline calicivirus[J].Ann NY Acad Sci,2003,1010(1):587-590.
[14]Abente E J,Sosnovtsev S V,Sandoval-Jaime C,Parra G I,Bok K,Green K Y.The feline calicivirus leader of the capsid protein is associated with cytopathic effect[J].J Virol,2013,87(6):3003-3017.
[15]Robinson B A,McCune B T,Peters A M,Nice T.Caspase-mediated cleavage of Murine Norovirus NS1/2potentiates apoptosis and is required for persistent infection[J].BioRxiv,2018:372615.
[16]Hyde J L,Mackenzie J M.Subcellular localization of the MNV-1 ORF1 proteins and their potential roles in the formation of the MNV-1 replication complex[J].Virology,2010,406(1):138-148.
[17]Furman L M,Maaty W S,Petersen L K,Ettayebi K,Hardy M E,Bothner B.Cysteine protease activation and apoptosis in Murine norovirus infection[J].Virol J,2009,6(1):139.
[18]Romero-Brey I,Bartenschlager R,Romero-Brey I,Bartenschlager R.Endoplasmic reticulum:the favorite intracellular niche for viral replication and assembly[J].Viruses,2016,8(6):160-160.
[19]Sharp T M,Guix S,Katayama K,Crawford S E,Estes M K.Inhibition of cellular protein secretion by norwalk virus nonstructural protein p22 requires a mimic of an endoplasmic reticulum export signal[J/OL].PLoSOne,2010,5(10):e13130.
[20]Urakova N,Frese M,Hall R N,Liu J,Matthaei M,Strive T.Expression and partial characterisation of rabbit haemorrhagic disease virus non-structural proteins[J].Virology,2015,484:69-79.
[21]udshoorn D,Hoeven B van der,Limpens R W A L,Beugeling C,Snijder E J,Bárcena M,Kikkert M.Antiviral innate immune response interferes with the formation of replication-associated membrane structures induced by a positive-strand RNA virus[J/OL].MBio,2016,7(6):e 01991-16.
[22]Wang M,Kaufman R J.Protein misfolding in the endoplasmic reticulum as a conduit to human disease[J].Nature,2016,529(7586):326-335.
[23]Hetz C,Papa F R.The unfolded protein response and cell fate control[J].Mol Cell,2018,69(2):169-181.
[24]Bailey D,Kaiser W J,Hollinshead M,Moffat K,Chaudhry Y,Wileman T,Sosnovtsev S V,Goodfellow I G.Feline calicivirus p32,p39 and p30 proteins localize to the endoplasmic reticulum to initiate replication complex formation[J].J Gen Virol,2010,91(3):739-749.
[25]Alvarez-Sanchez C,Cancio-Lonches C,Mora-Heredia JE,Santos-Valencia J C,Barrera-Vázquez O S,Yocupicio-Monroy M.Negative effect of heat shock on feline calicivirus release from infected cells is associated with the control of apoptosis[J].Virus Res,2015,198:44-52.
[26]Humoud M N,Doyle N,Royall E,Willcocks M M,Sorgeloos F,Kuppeveld F van,Roberts L O,Goodfellow I G,Langereis M A,Locker N.Feline Calicivirus infection disrupts the assembly of cytoplasmic stress granules and induces G3BP1 cleavage[J].J Virol,2016,90(14):6489-6501.
[27]Dickens L S,Powley I R,Hughes M A,MacFarlane M.The‘complexities’of life and death:Death receptor signalling platforms[J].Exp Cell Res,2012,318(11):1269-1277.
[28]Galluzzi L,Vitale I,Aaronson S A,et al.Molecular mechanisms of cell death:recommendations of the Nomenclature Committee on Cell Death 2018[J].Cell Death Differ,2018,25(3):486-541.
[29]Newton K,Dixit V M.Signaling in innate immunity and inflammation[J].Cold Spring Harb Perspect Bio,2012,4(3):a006049-a006049.
[30]Bousoik E,Montazeri Aliabadi H.“Do We Know Jack”about JAK?A closer look at JAK/STAT signaling pathway[J].Front Oncol,2018,8:287-287.
[31]刘永相.猫杯状病毒感染抑制Ⅰ型干扰素信号通路的分子机制[D].中国农业科学院,2018.
[32]Rongvaux A,Jackson R,Harman C C D,Li T,West A P,de Zoete M R,Wu Y,Yordy B,Lakhani S A,Kuan C-Y,Taniguchi T,Shadel G S,Chen Z J,Iwasaki A,Flavell R A.Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA[J].Cell,2014,159(7):1563-1577.
[33]Chattopadhyay S,Marques J T,Yamashita M,Peters K L,Smith K,Desai A,Williams B R G,Sen G C.Viral apoptosis is induced by IRF-3-mediated activation of Bax[J].EMBO J,2010,29(10):1762-1773.
[34]Yumiketa Y,Narita T,Inoue Y,Sato G,Kamitani W,Oka T,Katayama K,Sakaguchi T,Tohya Y.Nonstructural protein p39 of feline calicivirus suppresses host innate immune response by preventing IRF-3 activation[J].Vet Microbiol,2016,185:62-67.
[35]Jeong S I,Kim J W,Ko K P,Ryu B K,Lee M G,Kim H J,Chi S G.XAF1 forms a positive feedback loop with IRF-1 to drive apoptotic stress response and suppress tumorigenesis[J].Cell Death Dis,2018,9(8):806-806.
[36]Liu Y,Liu X,Kang H,Hu X,Liu J,Tian J,Qu L.Identification of feline interferon regulatory factor 1 as an efficient antiviral factor against the replication of feline calicivirus and other feline viruses[J].Biomed Res Int,2018,1-10.
[37]Alfajaro M M,Choi J S,Kim D S,Seo J Y,Kim J Y,Park J G,Soliman M,Baek Y B,Cho E H,Kwon J,Kwon H J,Park S J,Lee W S,Kang M I,Hosmillo M,Goodfellow I,Cho K O.Activation of COX-2/PGE2 promotes sapovirus replication via the inhibition of nitric oxide production[J].J Virol,2017,91(3):01656-01656.
[38]Alfajaro M M,Cho E H,Park J G,Kim J Y,Soliman M,Baek Y B,Kang M I,Park S I,Cho K O.Feline calicivirus-and murine norovirus-induced COX-2/PGE2signaling pathway has proviral effects[J/OL].PLoSOne,2018,13(7):e0200726.
[39]Akadera T,Yumoto H,Tozuka Y,Ohyashiki T.Prostaglandin E2 induces caspase-dependent apoptosis in rat cortical cells[J].Neurosci Lett,2002,317(2):61-64.