PDF(Pubmed)
Abstract：
Hepatitis B virus (HBV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Despite the advent of vaccines and potent antiviral agents able to suppress viral replication, recovery from chronic HBV infection is still an extremely difficult goal to achieve. Complex interactions between virus and host are responsible for HBV persistence and the risk of oncogenesis. Through multiple pathways, HBV is able to silence both innate and adaptive immunological responses and become out of control. Furthermore, the integration of the viral genome into that of the host and the production of covalently closed circular DNA (cccDNA) represent reservoirs of viral persistence and account for the difficult eradication of the infection. An adequate knowledge of the virus-host interaction mechanisms responsible for viral persistence and the risk of hepatocarcinogenesis is necessary for the development of functional cures for chronic HBV infection. The purpose of this review is, therefore, to analyze how interactions between HBV and host concur in the mechanisms of infection, persistence, and oncogenesis and what are the implications and the therapeutic perspectives that follow.
摘要：
乙型肝炎病毒(HBV)是慢性肝炎的主要病因,肝硬化,和肝细胞癌。尽管出现了能够抑制病毒复制的疫苗和有效的抗病毒药物，从慢性HBV感染中恢复仍然是一个极其困难的目标。病毒和宿主之间的复杂相互作用是造成HBV持久性和肿瘤发生风险的原因。通过多种途径，HBV能够沉默先天和适应性免疫反应，并失去控制。此外，病毒基因组整合到宿主的基因组和共价闭合环状DNA（cccDNA）的产生代表了病毒持久性的储库，并解释了感染的难以根除。对负责病毒持久性和肝癌发生风险的病毒-宿主相互作用机制的充分了解对于慢性HBV感染的功能性治疗的发展是必要的。这次审查的目的是,因此,分析HBV与宿主之间的相互作用如何在感染机制中发挥作用，持久性,和肿瘤发生，以及接下来的含义和治疗观点。
