Hepatitis C virus and antiviral innate immunity: Who wins at tug-of-war?

被引:23
作者
Yang, Da-Rong [1 ]
Zhu, Hai-Zhen [1 ,2 ]
机构
[1] Hunan Univ, Dept Mol Med Coll Biol, State Key Lab Chemo Biosensing & Chemometr, Changsha 410082, Hunan, Peoples R China
[2] Cent South Univ, Res Ctr Canc Prevent & Treatment, Translat Med Res Ctr Liver Canc, Hunan Prov Tumor Hosp,Affiliated Tumor Hosp,Xiang, Changsha 410013, Hunan, Peoples R China
关键词
Hepatitis C virus; Interferon; Interferon-stimulated gene; RIG-I; Toll-like receptor; Virus-host interaction; Chronic hepatitis; Immune evasion; Cell culture system for hepatitis C virus; INTERFERON-STIMULATED GENES; HUMANIZED MOUSE MODEL; CELL-CULTURE SYSTEMS; E3 UBIQUITIN LIGASE; TOLL-LIKE RECEPTORS; PROTEIN-KINASE PKR; B TYPE-I; RIG-I; 2'; 5'-OLIGOADENYLATE SYNTHETASE; COMPLETE REPLICATION;
D O I
10.3748/wjg.v21.i13.3786
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Hepatitis C virus (HCV) is a major human pathogen of chronic hepatitis and related liver diseases. Innate immunity is the first line of defense against invading foreign pathogens, and its activation is dependent on the recognition of these pathogens by several key sensors. The interferon (IFN) system plays an essential role in the restriction of HCV infection via the induction of hundreds of IFN-stimulated genes (ISGs) that inhibit viral replication and spread. However, numerous factors that trigger immune dysregulation, including viral factors and host genetic factors, can help HCV to escape host immune response, facilitating viral persistence. In this review, we aim to summarize recent advances in understanding the innate immune response to HCV infection and the mechanisms of ISGs to suppress viral survival, as well as the immune evasion strategies for chronic HCV infection.
引用
收藏
页码:3786 / 3800
页数:15
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