脂质代谢在HCV感染及生命周期中的作用

徐楚; 张平安

doi:10.3969/j.issn.1001-5256.2019.02.035

脂质代谢在HCV感染及生命周期中的作用

DOI: 10.3969/j.issn.1001-5256.2019.02.035

徐楚,
张平安

武汉大学人民医院检验科

详细信息

中图分类号: R512.63
计量
- 文章访问数: 1678
- HTML全文浏览量: 33
- PDF下载量: 314
- 被引次数: 0
出版历程
- 收稿日期: 2018-07-30
- 出版日期: 2019-02-20

Research advances in the role of lipid metabolism in hepatitis C virus infection and life cycle

Department of Clinical Laboratory, Renmin Hospital of Wuhan University

摘要

摘要: HCV感染是导致机体发生肝硬化和终末期肝病甚至是肝癌的主要原因之一。HCV感染人体后,通常伴有胰岛素抵抗和脂代谢紊乱,引发一系列代谢综合征。目前仍没有有效的疫苗预防HCV感染,因此对HCV感染机制的探讨仍然是目前临床研究的重点。大量研究表明HCV感染与脂质之间存在复杂关系,但是脂质在HCV感染中的作用尚不清楚。综述了脂质代谢在HCV感染及生命周期中的作用,有助于了解肝脏内脂肪代谢异常及脂肪性肝病的发病机制。
- 肝炎病毒属 /
- 脂类代谢 /
- 综述
Abstract: Hepatitis C virus ( HCV) infection is one of the leading causes of liver cirrhosis, end-stage liver disease, and even liver cancer. Patients with HCV infection tend to have insulin resistance and dyslipidemia, which may lead to a series of metabolic syndromes and greatly threaten human health. At present, there are still no effective vaccines to prevent HCV infection, and therefore, the mechanism of HCV infection remains a hot topic in clinical research. Many studies have shown that there is a complex relationship between HCV infection and lipids, but the role of lipids in HCV infection remains unclear. This article reviews the current research status of the role of lipid metabolism in HCV infection and life cycle, in order to understand the mechanism of abnormal fat metabolism in the liver and the pathogenesis of fatty liver disease.
- hepacivirus /
- lipid metabolism /
- review

HTML全文

参考文献(40)

[1]van MEER G.Cellular lipidomics[J].EMBO J, 2005, 24 (18) :3159-3165.

[2]BANKWITZ D, DOEPKE M, HUEGING K, et al.Maturation of secreted HCV particles by incorporation of secreted ApoE protects from antibodies by enhancing infectivity[J].J Hepatol, 2017, 67 (3) :480-489.

[3]OLIVEIRA C, FOURNIER C, DESCAMPS V, et al.Apolipoprotein (a) inhibits hepatitis C virus entry through interaction with infectious particles[J].Hepatology, 2017, 65 (6) :1851-1864.

[4]GRAMMATIKOS G, FERREIROS N, BON D, et al.Variations in serum sphingolipid levels associate with liver fibrosis progression and poor treatment outcome in hepatitis C virus but not hepatitis B virus infection[J].Hepatology, 2015, 61 (3) :812-822.

[5]VALKOV I, IVANOVA R, ALEXIEV A, et al.Association of serum lipids with hepatic steatosis, stage of liver fibrosis and viral load in chronic hepatitis C[J].J Clin Diagn Res, 2017, 11 (8) :oc15-oc20.

[6]CHOO QL, KUO G, WEINER AJ, et al.Isolation of a cDNAclone derived from a blood-borne non-A, non-B viral hepatitis genome[J].Science, 1989, 244 (4902) :359-362.

[7]XU C, ZHANG PA.Research progress about hepatitis C virus infection and pattern recognition receptors[J].Occupation and Health, 2018, 34 (7) :1000-1004, 1009. (in Chinese) 徐楚, 张平安.慢性丙型肝炎病毒感染与模式识别受体的研究进展[J].职业与健康, 2018, 34 (7) :1000-1004, 1009.

[8]THRIFT AP, EL-SERAG HB, KANWAL F.Global epidemiology and burden of HCV infection and HCV-related disease[J].Nat Rev Gastroenterol Hepatol, 2017, 14 (2) :122.

[9]SHIMIZU K, SOROIDA Y, SATO M, et al.Eradication of hepatitis C virus is associated with the attenuation of steatosis as evaluated using a controlled attenuation parameter[J].Sci Rep, 2018, 8 (1) :7845.

[10]KAITO M, WATANABE S, TSUKIYAMA-KOHARA K, et al.Hepatitis C virus particle detected by immunoelectron microscopic study[J].J Gen Virol, 1994, 75 (7) :1755-1760.

[11]GOODMAN ZD, ISHAK KG.Histopathology of hepatitis C virus infection[J].Semin Liver Dis, 1995, 15 (1) :70-81.

[12]MORIYA K, FUJIE H, SHINTANI Y, et al.The core protein of hepatitis C virus induces hepatocellular carcinoma in transgenic mice[J].Nat Med, 1998, 4 (9) :1065.

[13]PERLEMUTER G, SABILE A, LETTERON P, et al.Hepatitis C virus core protein inhibits microsomal triglyceride transfer protein activity and very low density lipoprotein secretion:A model of viral-related steatosis[J].FASEB J, 2002, 16 (2) :185-194.

[14]WAKITA T, PIETSCHMANN T, KATO T, et al.Production of infectious hepatitis C virus in tissue culture from a cloned viral genome[J].Nat Med, 2005, 11 (7) :791.

[15]MERZ A, LONG G, HIET MS, et al.Biochemical and morphological properties of hepatitis C virus particles and determination of their lipidome[J].J Biol Chem, 2010, 286 (4) :3018-3032.

[16]YAMAMOTO M, AIZAKI H, FUKASAWA M, et al.Structural requirements of virion-associated cholesterol for infectivity, buoyant density and apolipoprotein association of hepatitis Cvirus[J].J Gen Virol, 2011, 92 (9) :2082-2087.

[17]PIVER E, BOYER A, GAILLARD J, et al.Ultrastructural organisation of HCV from the bloodstream of infected patients revealed by electron microscopy after specific immunocapture[J].Gut, 2017, 66 (8) :1487-1495.

[18]XU Y, MARTINEZ P, SRON K, et al.Characterization of hepatitis C virus interaction with heparan sulfate proteoglycans[J].J Virol, 2015, 89 (7) :3846-3858.

[19]MOLINA S, CASTET V, FOURNIER-WIRTH C, et al.The low-density lipoprotein receptor plays a role in the infection of primary human hepatocytes by hepatitis C virus[J].J Hepatol, 2007, 46 (3) :411-419.

[20]ALBECKA A, BELOUZARD S, DE BEECK AO, et al.Role of low-density lipoprotein receptor in the hepatitis C virus life cycle[J].Hepatology, 2012, 55 (4) :998-1007.

[21]SHEN WJ, HU J, HU Z, et al.Scavenger receptor class Btype I (SR-BI) :A versatile receptor with multiple functions and actions[J].Metabolism, 2014, 63 (7) :875-886.

[22]SCARSELLI E, ANSUINI H, CERINO R, et al.The human scavenger receptor class B type I is a novel candidate receptor for the hepatitis C virus[J].EMBO J, 2002, 21 (19) :5017-5025.

[23]THI VLD, GRANIER C, ZEISEL MB, et al.Characterization of hepatitis C virus particle sub-populations reveals multiple usage of the scavenger receptor BI for entry steps[J].J Biol Chem, 2012, 287 (37) :31242-31257.

[24]SAINZ JR B, BARRETTO N, MARTIN DN, et al.Identification of the Niemann-Pick C1-like 1 cholesterol absorption receptor as a new hepatitis C virus entry factor[J].Nat Med, 2012, 18 (2) :281.

[25]REGHELLIN V, DONNICI L, FENU S, et al.NS5A inhibitors impair NS5A-PI4KIIIαcomplex formation and cause a decrease of PI4P and cholesterol levels in HCV-associated membranes[J].Antimicrob Agents Chemother, 2014, 58 (12) :7128-7140.

[26]BERGER KL, COOPER JD, HEATON NS, et al.Roles for endocytic trafficking and phosphatidylinositol 4-kinase III alpha in hepatitis C virus replication[J].Proc Natl Acad Sci U S A, 2009, 106 (18) :7577-7582.

[27]LIM YS, HWANG SB.Hepatitis C virus NS5A protein interacts with phosphatidylinositol 4-kinase type IIIαand regulates viral propagation[J].J Biol Chem, 2011, 286 (13) :11290-111298.

[28]DOROBANTU CM, ALBULESCU L, HARAK C, et al.Modulation of the host lipid landscape to promote RNA virus replication:the picornavirus encephalomyocarditis virus converges on the pathway used by hepatitis C virus[J].PLo S Pathog, 2015, 11 (9) :e1005185.

[29]WANG H, TAI AW.Mechanisms of cellular membrane reorganization to support hepatitis C virus replication[J].Viruses, 2016, 8 (5) :142.

[30]SU AI, PEZACKI JP, WODICKA L, et al.Genomic analysis of the host response to hepatitis C virus infection[J].Proc Natl Acad Sci U S A, 2002, 99 (24) :15669-15674.

[31]KAPADIA SB, CHISARI FV.Hepatitis C virus RNA replication is regulated by host geranylgeranylation and fatty acids[J].Proc Natl Acad Sci U S A, 2005, 102 (7) :2561-2566.

[32]YAMANE D, MCGIVERN DR, WAUTHIER E, et al.Regulation of the hepatitis C virus RNA replicase by endogenous lipid peroxidation[J].Nat Med, 2014, 20 (8) :927.

[33]CAMUS G, HERKER E, MODI AA, et al.Diacylglycerol glycerol acyltransferase-1 localizes hepatitis C virus NS5A protein to lipid droplets and enhances NS5A interaction with the viral capsid core[J].J Biol Chem, 2013, 288 (14) :9915-9923.

[34]COTTAREL J, PLISSONNIER ML, KULLOLLI M, et al.FIG4 is a hepatitis C virus particle-bound protein implicated in virion morphogenesis and infectivity with cholesteryl ester modulation potential[J].J Gen Virol, 2016, 97 (1) :69-81.

[35]VIEYRES G, WELSCH K, GEROLD G, et al.ABHD5/CGI-58, the chanarin-dorfman syndrome protein, mobilises lipid stores for hepatitis C virus production[J].PLo S Pathog, 2016, 12 (4) :e1005568.

[36]WU JM, SKILL NJ, MALUCCIO MA.Evidence of aberrant lipid metabolism in hepatitis C and hepatocellular carcinoma[J].HPB, 2010, 12 (9) :625-636.

[37]MANNS MP, von HAHN T.Novel therapies for hepatitis C-one pill fits all?[J].Nat Rev Drug Discov, 2013, 12 (8) :595.

[38]AN ZY, DING Y, DOU XG.Selection and evaluation of treatment regimens with direct-acting antiviral agents for patients with chronic hepatitis C in the real world in China[J].J Clin Hepatol, 2018, 34 (2) :233-237. (in Chinese) 安子英, 丁洋, 窦晓光.我国慢性丙型肝炎患者真实世界中直接抗病毒药物治疗方案的选择与评价[J].临床肝胆病杂志, 2018, 34 (2) :233-237.

[39]ZHAO YN, LI H.Research advances in anti-hepatitis B virus targets[J].Int J Virol, 2017, 24 (3) :197-200. (in Chinese) 赵亚楠, 李红.抗乙型肝炎病毒靶点研究进展[J].国际病毒学杂志, 2017, 24 (3) :197-200.

[40]THI EP, MIRE CE, LEE AC, et al.Lipid nanoparticle siRNAtreatment of Ebola-virus-Makona-infected nonhuman primates[J].Nature, 2015, 521 (7552) :362.

施引文献

资源附件(0)

访问统计