Apoptosis in hepatitis C virus infection

被引:125
作者
Bantel, H [1 ]
Schulze-Osthoff, K [1 ]
机构
[1] Univ Dusseldorf, Inst Mol Med, D-40225 Dusseldorf, Germany
关键词
apoptosis; caspase; CD95; cytotoxic T lymphocyte; hepatitis; HCV; heptocellular carcinoma;
D O I
10.1038/sj.cdd.4401119
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Infection with hepatitis C virus (HCV) is characterized by inflammatory liver damage and a long viral persistence associated with an increased risk of developing hepatocellular carcinoma. Both in liver damage and in oncogenesis a disturbance of apoptosis has been implicated, although the underlying mechanisms in these apparently opposite processes are incompletely understood. HCV-triggered liver injury is mediated mainly by host immune mechanisms and eventually by direct cytopathic effects of HCV. Recent data shows that caspase activation, either triggered by death ligands, other cytokines, granzyme B or HCV proteins, is considerably upregulated in HCV-infected liver. Interestingly, caspase activation appears to correlate closely with the inflammatory response. Data about the role of single HCV proteins, either in cultured cells or transgenic animals models, however, are contradictory, as both pro- and anti-apoptotic effects have been observed. Nevertheless, apoptosis induction upon HCV infection may critically contribute to liver damage, while inhibition of apoptosis may result in HCV persistence and development of hepatocellular carcinoma.
引用
收藏
页码:S48 / S58
页数:11
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