E2 of hepatitis C virus inhibits apoptosis
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SCOPUS
- Title
- E2 of hepatitis C virus inhibits apoptosis
- Authors
- Lee, SH; Kim, YK; Kim, CS; Seol, SK; Kim, J; Cho, S; Song, YL; Bartenschlager, R; Jang, SK
- Date Issued
- 2005-12-15
- Publisher
- AMER ASSOC IMMUNOLOGISTS
- Abstract
- Hepatitis C virus (HCV) is the major causative agent of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma, and can be involved in very long chronic infections up to 30 years or more. Therefore, it has been speculated that HCV possesses mechanisms capable of modulating host defense systems such as innate and adaptive immunity. To investigate this virus-host interaction, we generated HCV replicons containing various HCV structural proteins and then analyzed the sensitivity of replicon-containing cells to the apoptosis-inducing agent, TRAIL. TRAIL-induced apoptosis was monitored by cleavage of procaspase-3 and procaspase-9 as well as that of their substrate poly(ADP-ribose) polymerase. TRAIL-induced apoptosis was inhibited in cells expressing HCV E2. Moreover, expression of HCV E2 enhanced the colony forming efficiency of replicon-containing cells by 25-fold. Blockage of apoptosis by E2 seems to be related to inhibition of TRAIL-induced cytochrome c release from the mitochondria. Based on these results, we propose that E2 augments persistent HCV infection by blocking host-induced apoptosis of infected cells.
- Keywords
- CORE PROTEIN INTERACTS; STRUCTURAL PROTEINS; CYTOCHROME-C; MEDIATED APOPTOSIS; SIGNALING PATHWAY; ENVELOPE PROTEIN; INDUCE APOPTOSIS; RNA REPLICATION; DECOY RECEPTORS; CELL-CULTURE
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/24273
- DOI
- 10.4049/jimmunol.175.12.8226
- ISSN
- 0022-1767
- Article Type
- Article
- Citation
- JOURNAL OF IMMUNOLOGY, vol. 175, no. 12, page. 8226 - 8235, 2005-12-15
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