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丙型肝炎病毒与免疫系统之间的相互作用。

Interaction between the hepatitis C virus and the immune system.

作者信息

Rehermann B

机构信息

Liver Diseases Section, NIDDK, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Semin Liver Dis. 2000;20(2):127-41. doi: 10.1055/s-2000-9946.

Abstract

The hepatitis C virus (HCV) causes a wide spectrum of liver diseases ranging from symptomatic or asymptomatic acute infection with self-limited disease to persistent infection with chronic active hepatitis and an increased risk of liver cirrhosis and hepatocellular carcinoma. The outcome of HCV infection (i.e., viral clearance or persistence) and the manifestation and degree of liver disease is the result of complicated interactions between the virus and the immune response of the host. Remarkably, most de novo HCV infections are clinically inapparent and characterized by a high incidence (70%) of chronically evolving hepatitis, which suggests that HCV may have evolved strategies to not induce, overcome, or evade efficient immune responses of the host. This may be a multifactorial process, influenced by viral tissue tropism, replication, sequence variation and by functional alteration of infected cells. The interaction between HCV and the specific humoral and cellular immune response of the host, the role of the liver as the primary site of viral replication, the target of the host's immune response, and potential mechanisms of viral escape are discussed.

摘要

丙型肝炎病毒(HCV)可引发一系列肝脏疾病,范围从伴有自限性疾病的有症状或无症状急性感染,到伴有慢性活动性肝炎的持续性感染,以及肝硬化和肝细胞癌风险增加。HCV感染的结果(即病毒清除或持续存在)以及肝脏疾病的表现和程度,是病毒与宿主免疫反应之间复杂相互作用的结果。值得注意的是,大多数新发HCV感染在临床上并不明显,其特征是慢性进展性肝炎的发生率很高(70%),这表明HCV可能已经进化出一些策略,以不诱导、克服或逃避宿主的有效免疫反应。这可能是一个多因素过程,受病毒组织嗜性、复制、序列变异以及受感染细胞功能改变的影响。本文讨论了HCV与宿主特异性体液和细胞免疫反应之间的相互作用、肝脏作为病毒复制主要部位的作用、宿主免疫反应的靶点以及病毒逃逸的潜在机制。

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