Hepatitis B virus biology and life cycle
Hepatitis B virus (HBV) specifically infects hepatocytes and causes severe liver diseases. The HBV life cycle is unique in that the genomic DNA (relaxed-circular partially double-stranded DNA: rcDNA) is converted to a molecular template DNA (covalently closed circular DNA: cccDNA) to amplify a viral...
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| Veröffentlicht in: | Antiviral research 2020-10, Vol.182, p.104925-104925, Article 104925 |
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| container_title | Antiviral research |
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| creator | Tsukuda, Senko Watashi, Koichi |
| description | Hepatitis B virus (HBV) specifically infects hepatocytes and causes severe liver diseases. The HBV life cycle is unique in that the genomic DNA (relaxed-circular partially double-stranded DNA: rcDNA) is converted to a molecular template DNA (covalently closed circular DNA: cccDNA) to amplify a viral RNA intermediate, which is then reverse-transcribed back to viral DNA. The highly stable characteristics of cccDNA result in chronic infection and a poor rate of cure. This complex life cycle of HBV offers a variety of targets to develop antiviral agents. We provide here an update on the current knowledge of HBV biology and its life cycle, which may help to identify new antiviral targets.
•HBV is a DNA virus that infects hepatocytes and replicates through an RNA intermediate.•HBV is a small virus that persists as an episome, covalently closed circular DNA (cccDNA) in the nucleus of infected cells.•HBV-host factor interactions required for viral replication have recently been clarified. |
| doi_str_mv | 10.1016/j.antiviral.2020.104925 |
| format | Article |
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•HBV is a DNA virus that infects hepatocytes and replicates through an RNA intermediate.•HBV is a small virus that persists as an episome, covalently closed circular DNA (cccDNA) in the nucleus of infected cells.•HBV-host factor interactions required for viral replication have recently been clarified.</description><identifier>ISSN: 0166-3542</identifier><identifier>EISSN: 1872-9096</identifier><identifier>DOI: 10.1016/j.antiviral.2020.104925</identifier><language>eng</language><publisher>Elsevier B.V</publisher><subject>cccDNA ; Entry ; HBV ; Life cycle ; NTCP ; Replication</subject><ispartof>Antiviral research, 2020-10, Vol.182, p.104925-104925, Article 104925</ispartof><rights>2020 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-2e795d70fe23ef47751fc07d06f4c7c4e68ac68e6eb3a5c35e41371573cfc2703</citedby><cites>FETCH-LOGICAL-c397t-2e795d70fe23ef47751fc07d06f4c7c4e68ac68e6eb3a5c35e41371573cfc2703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0166354220303399$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids></links><search><creatorcontrib>Tsukuda, Senko</creatorcontrib><creatorcontrib>Watashi, Koichi</creatorcontrib><title>Hepatitis B virus biology and life cycle</title><title>Antiviral research</title><description>Hepatitis B virus (HBV) specifically infects hepatocytes and causes severe liver diseases. The HBV life cycle is unique in that the genomic DNA (relaxed-circular partially double-stranded DNA: rcDNA) is converted to a molecular template DNA (covalently closed circular DNA: cccDNA) to amplify a viral RNA intermediate, which is then reverse-transcribed back to viral DNA. The highly stable characteristics of cccDNA result in chronic infection and a poor rate of cure. This complex life cycle of HBV offers a variety of targets to develop antiviral agents. We provide here an update on the current knowledge of HBV biology and its life cycle, which may help to identify new antiviral targets.
•HBV is a DNA virus that infects hepatocytes and replicates through an RNA intermediate.•HBV is a small virus that persists as an episome, covalently closed circular DNA (cccDNA) in the nucleus of infected cells.•HBV-host factor interactions required for viral replication have recently been clarified.</description><subject>cccDNA</subject><subject>Entry</subject><subject>HBV</subject><subject>Life cycle</subject><subject>NTCP</subject><subject>Replication</subject><issn>0166-3542</issn><issn>1872-9096</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNqFkE1LAzEURYMoWKu_wVl2MzUfk2SyrEVboeBG1yF98yIp6UxNpoX-e6eMuHX14HLvgXcIeWR0zihTT7u5a_twCsnFOaf8klaGyysyYbXmpaFGXZPJ0FSlkBW_JXc57yilSpt6QmZrPLg-9CEXz8UAOeZiG7rYfZ0L1zZFDB4LOEPEe3LjXcz48Hun5PP15WO5Ljfvq7flYlOCMLovOWojG009coG-0loyD1Q3VPkKNFSoageqRoVb4SQIiRUTmkktwAPXVEzJbOQeUvd9xNzbfciAMboWu2O2vBJGcc6VGap6rELqck7o7SGFvUtny6i9uLE7--fGXtzY0c2wXIxLHD45BUw2Q8AWsAkJobdNF_5l_ADBL3AR</recordid><startdate>202010</startdate><enddate>202010</enddate><creator>Tsukuda, Senko</creator><creator>Watashi, Koichi</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202010</creationdate><title>Hepatitis B virus biology and life cycle</title><author>Tsukuda, Senko ; Watashi, Koichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-2e795d70fe23ef47751fc07d06f4c7c4e68ac68e6eb3a5c35e41371573cfc2703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>cccDNA</topic><topic>Entry</topic><topic>HBV</topic><topic>Life cycle</topic><topic>NTCP</topic><topic>Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsukuda, Senko</creatorcontrib><creatorcontrib>Watashi, Koichi</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Antiviral research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsukuda, Senko</au><au>Watashi, Koichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatitis B virus biology and life cycle</atitle><jtitle>Antiviral research</jtitle><date>2020-10</date><risdate>2020</risdate><volume>182</volume><spage>104925</spage><epage>104925</epage><pages>104925-104925</pages><artnum>104925</artnum><issn>0166-3542</issn><eissn>1872-9096</eissn><abstract>Hepatitis B virus (HBV) specifically infects hepatocytes and causes severe liver diseases. The HBV life cycle is unique in that the genomic DNA (relaxed-circular partially double-stranded DNA: rcDNA) is converted to a molecular template DNA (covalently closed circular DNA: cccDNA) to amplify a viral RNA intermediate, which is then reverse-transcribed back to viral DNA. The highly stable characteristics of cccDNA result in chronic infection and a poor rate of cure. This complex life cycle of HBV offers a variety of targets to develop antiviral agents. We provide here an update on the current knowledge of HBV biology and its life cycle, which may help to identify new antiviral targets.
•HBV is a DNA virus that infects hepatocytes and replicates through an RNA intermediate.•HBV is a small virus that persists as an episome, covalently closed circular DNA (cccDNA) in the nucleus of infected cells.•HBV-host factor interactions required for viral replication have recently been clarified.</abstract><pub>Elsevier B.V</pub><doi>10.1016/j.antiviral.2020.104925</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0166-3542 |
| ispartof | Antiviral research, 2020-10, Vol.182, p.104925-104925, Article 104925 |
| issn | 0166-3542 1872-9096 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2439622269 |
| source | ScienceDirect Journals (5 years ago - present) |
| subjects | cccDNA Entry HBV Life cycle NTCP Replication |
| title | Hepatitis B virus biology and life cycle |
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