Cellular and molecular interactions in coinfection with hepatitis C virus and human immunodeficiency virus

Cellular and molecular interactions in coinfection with hepatitis C virus and human immunodeficiency virus
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DOI:
10.1017/s1462399408000847
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发表时间:
2008-10
影响因子:
6.2
通讯作者:
B. Roe;W. Hall
B. Roe;W. Hall
中科院分区:
医学2区
文献类型:
--
作者:
B. Roe;W. Hall

文献摘要

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丙型肝炎病毒(HCV)和人类免疫缺陷病毒(HIV)的合并感染与HCV复制增加和更迅速发展为严重肝脏疾病相关,包括肝硬化和肝细胞癌的发展。在这篇综述中,我们讨论了目前对HCV/HIV合并感染的发病机制以及与肝病加速病程相关的细胞和分子机制的理解。与单独感染HCV的患者相比,HCV/HIV合并感染患者的HCV特异性t细胞应答的强度和广度降低,这表明HIV诱导的免疫抑制损害了对HCV的免疫应答。HCV不是直接的细胞病变,但在感染患者的肝脏中观察到的许多病理变化是肝内抗病毒免疫反应的直接结果。细胞凋亡还通过诱导涉及宿主免疫反应和HCV病毒蛋白的凋亡途径在HCV介导的肝损伤中发挥作用。本文综述了HCV/ hiv合并感染患者中细胞介导的免疫反应和细胞凋亡与肝脏疾病进展相关的证据。
Coinfection with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) is associated with increased HCV replication and a more rapid progression to severe liver disease, including the development of cirrhosis and hepatocellular carcinoma. In this review, we discuss the current understanding of the pathogenesis of HCV/HIV coinfection and the cellular and molecular mechanisms associated with the accelerated course of liver disease. The strength and breadth of HCV-specific T-cell responses are reduced in HCV/HIV-coinfected patients compared with those infected with HCV alone, suggesting that the immunosuppression induced by HIV compromises immune responses to HCV. HCV is not directly cytopathic, but many of the pathological changes observed in the liver of infected patients are a direct result of the intrahepatic antiviral immune responses. Apoptosis also has a role in HCV-mediated liver damage through the induction of apoptotic pathways involving the host immune response and HCV viral proteins. This review summarises the evidence correlating the role of cell-mediated immune responses and apoptosis with liver disease progression in HCV/HIV-coinfected patients.