HCV Innate Immune Responses

被引：4
作者：
Heim, Markus H. [1 ,2 ]
机构：
[1] Univ Basel Hosp, Clin Gastroenterol & Hepatol, CH-4031 Basel, Switzerland
[2] Univ Basel, Dept Biomed, ZLF, CH-4031 Basel, Switzerland
来源：
VIRUSES-BASEL | 2009年 / 1卷 / 03期
关键词：
interferon; MAVS; Toll-like receptors; Jak-STAT; HCV; viral interference; HEPATITIS-C VIRUS; INTERFERON-GAMMA RECEPTOR; PROTEIN-TYROSINE-PHOSPHATASE; TOLL-LIKE RECEPTOR-3; DOUBLE-STRANDED-RNA; NF-KAPPA-B; INHIBITS INTERFERON; RIG-I; VIRAL-INFECTION; ADAPTER PROTEIN;
D O I：
10.3390/v1031073
中图分类号：
Q93 [微生物学];
学科分类号：
071005 ; 100705 ;
摘要：
Hepatitis C virus (HCV) establishes a persistent infection in more than 70% of infected individuals. This striking ability to evade the powerful innate immune system results from viral interference occurring at several levels of the interferon (IFN) system. There is strong evidence from cell culture experiments that HCV can inhibit the induction of IFN beta by cleaving important proteins in the virus sensory pathways of cells such as MAVS and TRIF. There is also evidence that HCV interferes with IFN alpha signaling through the Jak-STAT pathway, and that HCV proteins target IFN effector systems such as protein kinase R (PKR). These in vitro findings will have to be confirmed in clinical trials investigating the molecular mechanisms of HCV interference with the innate immune system in liver samples.
引用
收藏
页码：1073 / 1088
页数：16
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