E2 of hepatitis C virus inhibits apoptosis

Song Hee Lee, Yoon Ki Kim, Chon Saeng Kim, Su Kyoung Seol, Joonhyun Kim, Sungchan Cho, Young Lan Song, Ralf Bartenschlager, Sung Key Jang

Research output: Contribution to journalArticlepeer-review

71 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)8226-8235
Number of pages10
JournalJournal of Immunology
Issue number12
Publication statusPublished - 2005 Dec 15
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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