E2 of Hepatitis C Virus Inhibits Apoptosis
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 sys...
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| Veröffentlicht in: | Journal of Immunology 2005-12, Vol.175 (12), p.8226-8235 |
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| container_issue | 12 |
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| container_title | Journal of Immunology |
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| creator | Lee, Song Hee Kim, Yoon Ki Kim, Chon Saeng Seol, Su Kyoung Kim, Joonhyun Cho, Sungchan Song, Young Lan Bartenschlager, Ralf Jang, Sung Key |
| description | 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. |
| doi_str_mv | 10.4049/jimmunol.175.12.8226 |
| format | Article |
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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.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.4049/jimmunol.175.12.8226</identifier><identifier>PMID: 16339562</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Apoptosis ; Apoptosis Regulatory Proteins - physiology ; Carcinoma, Hepatocellular - pathology ; Cell Line, Tumor ; Cytochromes c - metabolism ; Hepatitis C - etiology ; Hepatitis C - pathology ; Hepatitis C virus ; Humans ; Membrane Glycoproteins - physiology ; Mitochondrial Proteins - metabolism ; Replicon - genetics ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Necrosis Factor-alpha - physiology ; Viral Envelope Proteins - physiology ; Viral Proteins - genetics ; Viral Proteins - physiology</subject><ispartof>Journal of Immunology, 2005-12, Vol.175 (12), p.8226-8235</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-7e21f42158fbadcc7c7b1b2ba93e047251887f74ecd3e5d83e7bf8c19776c8753</citedby><cites>FETCH-LOGICAL-c481t-7e21f42158fbadcc7c7b1b2ba93e047251887f74ecd3e5d83e7bf8c19776c8753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16339562$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Song Hee</creatorcontrib><creatorcontrib>Kim, Yoon Ki</creatorcontrib><creatorcontrib>Kim, Chon Saeng</creatorcontrib><creatorcontrib>Seol, Su Kyoung</creatorcontrib><creatorcontrib>Kim, Joonhyun</creatorcontrib><creatorcontrib>Cho, Sungchan</creatorcontrib><creatorcontrib>Song, Young Lan</creatorcontrib><creatorcontrib>Bartenschlager, Ralf</creatorcontrib><creatorcontrib>Jang, Sung Key</creatorcontrib><title>E2 of Hepatitis C Virus Inhibits Apoptosis</title><title>Journal of Immunology</title><addtitle>J Immunol</addtitle><description>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.</description><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - physiology</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cytochromes c - metabolism</subject><subject>Hepatitis C - etiology</subject><subject>Hepatitis C - pathology</subject><subject>Hepatitis C virus</subject><subject>Humans</subject><subject>Membrane Glycoproteins - physiology</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Replicon - genetics</subject><subject>Signal Transduction</subject><subject>TNF-Related Apoptosis-Inducing Ligand</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><subject>Viral Envelope Proteins - physiology</subject><subject>Viral Proteins - genetics</subject><subject>Viral Proteins - physiology</subject><issn>0022-1767</issn><issn>1550-6606</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1Kw0AYRQdRbK2-gUhWIkLifPOfpZRqCwU36naYTCZ2StLETELw7U1pRXeu7ubcszgIXQNOGGbpw9ZXVb-rywQkT4AkihBxgqbAOY6FwOIUTTEmJAYp5ARdhLDFGAtM2DmagKA05YJM0f2CRHURLV1jOt_5EM2jd9_2IVrtNj7zXYgem7rp6uDDJTorTBnc1XFn6O1p8TpfxuuX59X8cR1bpqCLpSNQMAJcFZnJrZVWZpCRzKTUYSYJB6VkIZmzOXU8V9TJrFAWUimFVZLTGbo9eJu2_uxd6HTlg3VlaXau7oMWSilOGfwLgmQk5RSPIDuAtq1DaF2hm9ZXpv3SgPU-pv6JOX64BqL3McfbzdHfZ5XLf0_HeiNwdwA2_mMz-NbpUJmyHHHQwzD8dX0DJ5h-Ww</recordid><startdate>20051215</startdate><enddate>20051215</enddate><creator>Lee, Song Hee</creator><creator>Kim, Yoon Ki</creator><creator>Kim, Chon Saeng</creator><creator>Seol, Su Kyoung</creator><creator>Kim, Joonhyun</creator><creator>Cho, Sungchan</creator><creator>Song, Young Lan</creator><creator>Bartenschlager, Ralf</creator><creator>Jang, Sung Key</creator><general>Am Assoc Immnol</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20051215</creationdate><title>E2 of Hepatitis C Virus Inhibits Apoptosis</title><author>Lee, Song Hee ; Kim, Yoon Ki ; Kim, Chon Saeng ; Seol, Su Kyoung ; Kim, Joonhyun ; Cho, Sungchan ; Song, Young Lan ; Bartenschlager, Ralf ; Jang, Sung Key</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-7e21f42158fbadcc7c7b1b2ba93e047251887f74ecd3e5d83e7bf8c19776c8753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - physiology</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cytochromes c - metabolism</topic><topic>Hepatitis C - etiology</topic><topic>Hepatitis C - pathology</topic><topic>Hepatitis C virus</topic><topic>Humans</topic><topic>Membrane Glycoproteins - physiology</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Replicon - genetics</topic><topic>Signal Transduction</topic><topic>TNF-Related Apoptosis-Inducing Ligand</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><topic>Viral Envelope Proteins - physiology</topic><topic>Viral Proteins - genetics</topic><topic>Viral Proteins - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Song Hee</creatorcontrib><creatorcontrib>Kim, Yoon Ki</creatorcontrib><creatorcontrib>Kim, Chon Saeng</creatorcontrib><creatorcontrib>Seol, Su Kyoung</creatorcontrib><creatorcontrib>Kim, Joonhyun</creatorcontrib><creatorcontrib>Cho, Sungchan</creatorcontrib><creatorcontrib>Song, Young Lan</creatorcontrib><creatorcontrib>Bartenschlager, Ralf</creatorcontrib><creatorcontrib>Jang, Sung Key</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Song Hee</au><au>Kim, Yoon Ki</au><au>Kim, Chon Saeng</au><au>Seol, Su Kyoung</au><au>Kim, Joonhyun</au><au>Cho, Sungchan</au><au>Song, Young Lan</au><au>Bartenschlager, Ralf</au><au>Jang, Sung Key</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>E2 of Hepatitis C Virus Inhibits Apoptosis</atitle><jtitle>Journal of Immunology</jtitle><addtitle>J Immunol</addtitle><date>2005-12-15</date><risdate>2005</risdate><volume>175</volume><issue>12</issue><spage>8226</spage><epage>8235</epage><pages>8226-8235</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><eissn>1365-2567</eissn><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. 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| subjects | Apoptosis Apoptosis Regulatory Proteins - physiology Carcinoma, Hepatocellular - pathology Cell Line, Tumor Cytochromes c - metabolism Hepatitis C - etiology Hepatitis C - pathology Hepatitis C virus Humans Membrane Glycoproteins - physiology Mitochondrial Proteins - metabolism Replicon - genetics Signal Transduction TNF-Related Apoptosis-Inducing Ligand Tumor Necrosis Factor-alpha - physiology Viral Envelope Proteins - physiology Viral Proteins - genetics Viral Proteins - physiology |
| title | E2 of Hepatitis C Virus Inhibits Apoptosis |
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