early autophagic pathway is activated by hepatitis B virus and required for viral DNA replication
Autophagy is a catabolic process by which cells remove long-lived proteins and damaged organelles for recycling. Viral infections may also induce autophagic response. Here we show that hepatitis B virus (HBV), a pathogen that chronically infects [almost equal to]350 million people globally, can enha...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2010-03, Vol.107 (9), p.4383-4388 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Sir, Donna Tian, Yongjun Chen, Wen-ling Ann, David K Yen, Tien-Sze Benedict Ou, Jing-hsiung James |
| description | Autophagy is a catabolic process by which cells remove long-lived proteins and damaged organelles for recycling. Viral infections may also induce autophagic response. Here we show that hepatitis B virus (HBV), a pathogen that chronically infects [almost equal to]350 million people globally, can enhance autophagic response in cell cultures, mouse liver, and during natural infection. This enhancement of the autophagic response is not coupled by an increase of autophagic protein degradation and is dependent on the viral X protein, which binds to and enhances the enzymatic activity of phosphatidylinositol 3-kinase class III, an enzyme critical for the initiation of autophagy. Further analysis indicates that autophagy enhances HBV DNA replication, with minimal involvement of late autophagic vacuoles in this process. Our studies thus demonstrate that a DNA virus can use autophagy to enhance its own replication and indicate the possibility of targeting the autophagic pathway for the treatment of HBV patients. |
| doi_str_mv | 10.1073/pnas.0911373107 |
| format | Article |
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Viral infections may also induce autophagic response. Here we show that hepatitis B virus (HBV), a pathogen that chronically infects [almost equal to]350 million people globally, can enhance autophagic response in cell cultures, mouse liver, and during natural infection. This enhancement of the autophagic response is not coupled by an increase of autophagic protein degradation and is dependent on the viral X protein, which binds to and enhances the enzymatic activity of phosphatidylinositol 3-kinase class III, an enzyme critical for the initiation of autophagy. Further analysis indicates that autophagy enhances HBV DNA replication, with minimal involvement of late autophagic vacuoles in this process. Our studies thus demonstrate that a DNA virus can use autophagy to enhance its own replication and indicate the possibility of targeting the autophagic pathway for the treatment of HBV patients.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0911373107</identifier><identifier>PMID: 20142477</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Autophagy ; Base Sequence ; Binding sites ; Biological Sciences ; Blotting, Northern ; Blotting, Southern ; Cell culture ; Cell lines ; Cells, Cultured ; Deoxyribonucleic acid ; DNA ; DNA replication ; DNA, Viral - biosynthesis ; Enzyme Activation ; Genomes ; Hep G2 cells ; Hepatitis ; Hepatitis B ; Hepatitis B virus ; Hepatitis B virus - genetics ; Hepatitis B virus - physiology ; Hepatocytes ; Infections ; Kinases ; Liver cells ; Mice ; Phosphatidylinositol 3-Kinases - metabolism ; Proteins ; RNA ; RNA, Small Interfering ; Small interfering RNA ; Virus Replication</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2010-03, Vol.107 (9), p.4383-4388</ispartof><rights>Copyright National Academy of Sciences Mar 2, 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c586t-8435fc967a436545dbb9b3a3d65602422b5c647ad9b8f1c1ca8dfa5e0c46a5e43</citedby><cites>FETCH-LOGICAL-c586t-8435fc967a436545dbb9b3a3d65602422b5c647ad9b8f1c1ca8dfa5e0c46a5e43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/107/9.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/40537133$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/40537133$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20142477$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sir, Donna</creatorcontrib><creatorcontrib>Tian, Yongjun</creatorcontrib><creatorcontrib>Chen, Wen-ling</creatorcontrib><creatorcontrib>Ann, David K</creatorcontrib><creatorcontrib>Yen, Tien-Sze Benedict</creatorcontrib><creatorcontrib>Ou, Jing-hsiung James</creatorcontrib><title>early autophagic pathway is activated by hepatitis B virus and required for viral DNA replication</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Autophagy is a catabolic process by which cells remove long-lived proteins and damaged organelles for recycling. Viral infections may also induce autophagic response. Here we show that hepatitis B virus (HBV), a pathogen that chronically infects [almost equal to]350 million people globally, can enhance autophagic response in cell cultures, mouse liver, and during natural infection. This enhancement of the autophagic response is not coupled by an increase of autophagic protein degradation and is dependent on the viral X protein, which binds to and enhances the enzymatic activity of phosphatidylinositol 3-kinase class III, an enzyme critical for the initiation of autophagy. Further analysis indicates that autophagy enhances HBV DNA replication, with minimal involvement of late autophagic vacuoles in this process. Our studies thus demonstrate that a DNA virus can use autophagy to enhance its own replication and indicate the possibility of targeting the autophagic pathway for the treatment of HBV patients.</description><subject>Animals</subject><subject>Autophagy</subject><subject>Base Sequence</subject><subject>Binding sites</subject><subject>Biological Sciences</subject><subject>Blotting, Northern</subject><subject>Blotting, Southern</subject><subject>Cell culture</subject><subject>Cell lines</subject><subject>Cells, Cultured</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA replication</subject><subject>DNA, Viral - biosynthesis</subject><subject>Enzyme Activation</subject><subject>Genomes</subject><subject>Hep G2 cells</subject><subject>Hepatitis</subject><subject>Hepatitis B</subject><subject>Hepatitis B virus</subject><subject>Hepatitis B virus - genetics</subject><subject>Hepatitis B virus - physiology</subject><subject>Hepatocytes</subject><subject>Infections</subject><subject>Kinases</subject><subject>Liver cells</subject><subject>Mice</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proteins</subject><subject>RNA</subject><subject>RNA, Small Interfering</subject><subject>Small interfering RNA</subject><subject>Virus Replication</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1v1DAQxS0EomXhzAmIuHDa1p-xc6lUyqdUwQF6tiaOs-tVNk7tZNH-90y0ZVu4IB9Gfu83o7EfIS8ZPWNUi_Ohh3xGK8aEFig8IqcMb8tSVvQxOaWU66WRXJ6QZzlvKKWVMvQpOeGUoar1KQEPqdsXMI1xWMMquGKAcf0L9kXIBbgx7GD0TVHvi7VHJ4wovy92IU1o902R_O0UEhJtTLMMXfHh2yXKQxcc8rF_Tp600GX_4q4uyM2njz-vviyvv3_-enV5vXTKlCOuKVTrqlKDFKWSqqnrqhYgmlKVlEvOa-VKqaGpatMyxxyYpgXlqZMlFikW5OIwd5jqrW-c70fcxg4pbCHtbYRg_3b6sLaruLPcSMq4xgHv7gakeDv5PNptyM53HfQ-TtlqWXLBlKn-TwqBqDAUybf_kJs4pR7_wWIGQgqOZ0HOD5BLMefk2-PSjNo5ZjvHbO9jxo7XD9965P_k-gCYO-_HaVtZKYxA4NUB2OQxpiMhqRKaidl_c_BbiBZWKWR782NemTLDqGFa_AY3vcEN</recordid><startdate>20100302</startdate><enddate>20100302</enddate><creator>Sir, Donna</creator><creator>Tian, Yongjun</creator><creator>Chen, Wen-ling</creator><creator>Ann, David K</creator><creator>Yen, Tien-Sze Benedict</creator><creator>Ou, Jing-hsiung James</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</scope><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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100302</creationdate><title>early autophagic pathway is activated by hepatitis B virus and required for viral DNA replication</title><author>Sir, Donna ; 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| source | MEDLINE; JSTOR Archive Collection A-Z Listing; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | Animals Autophagy Base Sequence Binding sites Biological Sciences Blotting, Northern Blotting, Southern Cell culture Cell lines Cells, Cultured Deoxyribonucleic acid DNA DNA replication DNA, Viral - biosynthesis Enzyme Activation Genomes Hep G2 cells Hepatitis Hepatitis B Hepatitis B virus Hepatitis B virus - genetics Hepatitis B virus - physiology Hepatocytes Infections Kinases Liver cells Mice Phosphatidylinositol 3-Kinases - metabolism Proteins RNA RNA, Small Interfering Small interfering RNA Virus Replication |
| title | early autophagic pathway is activated by hepatitis B virus and required for viral DNA replication |
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