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丙型肝炎病毒与先天性和适应性免疫反应:共同进化与共存的故事

Hepatitis C virus versus innate and adaptive immune responses: a tale of coevolution and coexistence.

作者信息

Rehermann Barbara

机构信息

Immunology Section, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH/DHHS, Bethesda, MD 20892, USA.

出版信息

J Clin Invest. 2009 Jul;119(7):1745-54. doi: 10.1172/JCI39133. Epub 2009 Jul 1.

DOI:10.1172/JCI39133
PMID:19587449
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2701885/
Abstract

Since the identification of the hepatitis C virus (HCV) 20 years ago, much progress has been made in our understanding of its life cycle and interaction with the host immune system. Much has been learned from HCV itself, which, via decades of coevolution, gained an intricate knowledge of host innate and adaptive immune responses and developed sophisticated ways to preempt, subvert, and antagonize them. This review discusses the clinical, virological, and immunological features of acute and chronic hepatitis C and the role of the immune response in spontaneous and treatment-induced HCV clearance.

摘要

自20年前丙型肝炎病毒(HCV)被发现以来,我们对其生命周期以及与宿主免疫系统相互作用的理解取得了很大进展。从HCV自身我们了解到很多情况,经过数十年的共同进化,它对宿主的固有免疫和适应性免疫反应有了深入认识,并形成了先发制人、颠覆和对抗这些反应的复杂方式。本文综述了急性和慢性丙型肝炎的临床、病毒学和免疫学特征,以及免疫反应在自发清除和治疗诱导清除HCV中的作用。

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本文引用的文献

1
Selection pressure from neutralizing antibodies drives sequence evolution during acute infection with hepatitis C virus.在丙型肝炎病毒急性感染期间,来自中和抗体的选择压力驱动序列进化。
Gastroenterology. 2009 Jun;136(7):2377-86. doi: 10.1053/j.gastro.2009.02.080. Epub 2009 Mar 17.
2
Synergistic reversal of intrahepatic HCV-specific CD8 T cell exhaustion by combined PD-1/CTLA-4 blockade.通过联合阻断PD-1/CTLA-4协同逆转肝内丙型肝炎病毒特异性CD8 T细胞耗竭
PLoS Pathog. 2009 Feb;5(2):e1000313. doi: 10.1371/journal.ppat.1000313. Epub 2009 Feb 27.
3
PD-L1 negatively regulates CD4+CD25+Foxp3+ Tregs by limiting STAT-5 phosphorylation in patients chronically infected with HCV.在慢性丙型肝炎病毒感染患者中,程序性死亡受体配体1(PD-L1)通过限制信号转导子和转录激活子5(STAT-5)磷酸化对CD4+CD25+叉头框蛋白3+调节性T细胞(Tregs)产生负向调节作用。
J Clin Invest. 2009 Mar;119(3):551-64. doi: 10.1172/JCI36604. Epub 2009 Feb 23.
4
Analysis of CD8+ T-cell-mediated inhibition of hepatitis C virus replication using a novel immunological model.使用新型免疫模型分析CD8 + T细胞介导的丙型肝炎病毒复制抑制作用
Gastroenterology. 2009 Apr;136(4):1391-401. doi: 10.1053/j.gastro.2008.12.034. Epub 2008 Dec 13.
5
Human occludin is a hepatitis C virus entry factor required for infection of mouse cells.人闭锁蛋白是丙型肝炎病毒感染小鼠细胞所需的一种进入因子。
Nature. 2009 Feb 12;457(7231):882-6. doi: 10.1038/nature07684. Epub 2009 Jan 28.
6
Genomic analysis reveals a potential role for cell cycle perturbation in HCV-mediated apoptosis of cultured hepatocytes.基因组分析揭示了细胞周期紊乱在丙型肝炎病毒介导的培养肝细胞凋亡中的潜在作用。
PLoS Pathog. 2009 Jan;5(1):e1000269. doi: 10.1371/journal.ppat.1000269. Epub 2009 Jan 16.
7
Loss of viral fitness and cross-recognition by CD8+ T cells limit HCV escape from a protective HLA-B27-restricted human immune response.病毒适应性的丧失以及CD8 + T细胞的交叉识别限制了丙型肝炎病毒从保护性HLA - B27限制性人类免疫反应中逃逸。
J Clin Invest. 2009 Feb;119(2):376-86. doi: 10.1172/JCI36587. Epub 2009 Jan 12.
8
Natural killer cell function is intact after direct exposure to infectious hepatitis C virions.自然杀伤细胞在直接接触丙型肝炎感染性病毒粒子后功能保持完整。
Hepatology. 2009 Jan;49(1):12-21. doi: 10.1002/hep.22624.
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Toll-like receptor and RIG-I-like receptor signaling.Toll样受体和视黄酸诱导基因I样受体信号通路。
Ann N Y Acad Sci. 2008 Nov;1143:1-20. doi: 10.1196/annals.1443.020.
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Tight junction proteins claudin-1 and occludin control hepatitis C virus entry and are downregulated during infection to prevent superinfection.紧密连接蛋白claudin-1和闭合蛋白控制丙型肝炎病毒的进入,并且在感染期间下调以防止重复感染。
J Virol. 2009 Feb;83(4):2011-4. doi: 10.1128/JVI.01888-08. Epub 2008 Dec 3.