Host-virus interactions in hepatitis B virus infection

被引：125

作者：

Guidotti, Luca G. ^{[1
]}

Isogawa, Masanori ^{[2
]}

Chisari, Francis V. ^{[3
]}

机构：

[1] IRCCS San Raffaele Sci Inst, Div Immunol Transplantat & Infect Dis, I-20132 Milan, Italy

[2] Nagoya City Univ, Dept Virol, Grad Sch Med Sci, Mizuho Ku, Nagoya, Aichi 4678601, Japan

[3] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 2015年 / 36卷

基金：

欧洲研究理事会;

关键词：

TRANSGENIC MOUSE MODEL; CD8(+) T-CELLS; NATURAL-KILLER; HEPATOCELLULAR-CARCINOMA; IMMUNE-RESPONSE; VIRAL CLEARANCE; LIVER; REPLICATION; RECEPTOR; HBV;

D O I：

10.1016/j.coi.2015.06.016

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Hepatitis B virus (HBV) is a noncytopathic, hepatotropic, double-stranded DNA virus that causes acute and chronic hepatitis. Although HBV does not induce a measurable innate immune response in the infected liver, the outcome of infection is determined by the kinetics, breadth, vigor, trafficking, and effector functions of HBV-specific adaptive T cell responses, and the development of neutralizing antibodies. Dysregulation of one or more of these events leads to persistent HBV infection and a variably severe chronic necroinflammatory liver disease that fosters the development of hepatocellular carcinoma. Deeper understanding of the mechanisms responsible for immunological tolerance to HBV is needed in order to devise immunotherapeutic strategies to cure chronic HBV infection and prevent its life-threatening sequelae.

引用

页码：61 / 66

页数：6

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