A long-term follow-up analysis of serial core promoter and precore sequences in Japanese patients chronically infected by hepatitis B virus
To investigate the association of hepatitis B virus (HBV) with core promoter mutation (T1762A1764) or precore mutation (A1896) with the clinical course of illness, we analyzed serial core promoter and precore sequences in 22 patients with HBV-associated chronic liver disease who were followed for 12...
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| Veröffentlicht in: | Digestive diseases and sciences 2001-03, Vol.46 (3), p.509-515 |
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| creator | KAJIYA, Yuji HAMASAKI, Keisuke EGUCHI, Katsumi NAKATA, Keisuke MIYAZOE, Seiji TAKEDA, Yoshio HIGASHI, Shinichirou OHKUBO, Kazuaki ICHIKAWA, Tatsuki NAKAO, Kazuhiko KATO, Yuji |
| description | To investigate the association of hepatitis B virus (HBV) with core promoter mutation (T1762A1764) or precore mutation (A1896) with the clinical course of illness, we analyzed serial core promoter and precore sequences in 22 patients with HBV-associated chronic liver disease who were followed for 12+/-4 years (mean +/- SD). Sixteen of 22 patients were positive for HBeAg at baseline, and 15 of the 16 patients seroconverted to anti-HBe during the observation period. T1762A1764 mutation was detected in 16 of 22 patients, including 11 patients positive for HBeAg, at baseline. During the follow-up period, A1896 mutation emerged in 7 of 16 patients who had the wild-type HBV or only the T1762A1764 mutation at baseline. Sustained remission of hepatitis correlated with the low level of viremia, but did not with type of mutations. These results indicate that HBV with T1762A1764 mutation tends to precede A1896 mutation during the course of infection in Japanese patients with chronic liver disease. |
| doi_str_mv | 10.1023/A:1005582812466 |
| format | Article |
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Sixteen of 22 patients were positive for HBeAg at baseline, and 15 of the 16 patients seroconverted to anti-HBe during the observation period. T1762A1764 mutation was detected in 16 of 22 patients, including 11 patients positive for HBeAg, at baseline. During the follow-up period, A1896 mutation emerged in 7 of 16 patients who had the wild-type HBV or only the T1762A1764 mutation at baseline. Sustained remission of hepatitis correlated with the low level of viremia, but did not with type of mutations. These results indicate that HBV with T1762A1764 mutation tends to precede A1896 mutation during the course of infection in Japanese patients with chronic liver disease.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1023/A:1005582812466</identifier><identifier>PMID: 11318524</identifier><identifier>CODEN: DDSCDJ</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Adult ; Base Sequence ; Biological and medical sciences ; Female ; Follow-Up Studies ; Hepatitis B Antibodies - blood ; Hepatitis B e Antigens - blood ; Hepatitis B virus - genetics ; Hepatitis B, Chronic - virology ; Human viral diseases ; Humans ; Infectious diseases ; Kruppel-Like Factor 6 ; Kruppel-Like Transcription Factors ; Male ; Medical sciences ; Middle Aged ; Mutation ; Polymerase Chain Reaction ; Proto-Oncogene Proteins ; Trans-Activators - blood ; Trans-Activators - genetics ; Viral diseases ; Viral hepatitis</subject><ispartof>Digestive diseases and sciences, 2001-03, Vol.46 (3), p.509-515</ispartof><rights>2001 INIST-CNRS</rights><rights>Copyright Kluwer Academic Publishers Mar 2001</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c308t-60dc96e9a5db8edee509c36f7032dbc770bd925cf927ed818787f31d093abeea3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,777,781,786,787,23911,23912,25121,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=981062$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11318524$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KAJIYA, Yuji</creatorcontrib><creatorcontrib>HAMASAKI, Keisuke</creatorcontrib><creatorcontrib>EGUCHI, Katsumi</creatorcontrib><creatorcontrib>NAKATA, Keisuke</creatorcontrib><creatorcontrib>MIYAZOE, Seiji</creatorcontrib><creatorcontrib>TAKEDA, Yoshio</creatorcontrib><creatorcontrib>HIGASHI, Shinichirou</creatorcontrib><creatorcontrib>OHKUBO, Kazuaki</creatorcontrib><creatorcontrib>ICHIKAWA, Tatsuki</creatorcontrib><creatorcontrib>NAKAO, Kazuhiko</creatorcontrib><creatorcontrib>KATO, Yuji</creatorcontrib><title>A long-term follow-up analysis of serial core promoter and precore sequences in Japanese patients chronically infected by hepatitis B virus</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><description>To investigate the association of hepatitis B virus (HBV) with core promoter mutation (T1762A1764) or precore mutation (A1896) with the clinical course of illness, we analyzed serial core promoter and precore sequences in 22 patients with HBV-associated chronic liver disease who were followed for 12+/-4 years (mean +/- SD). Sixteen of 22 patients were positive for HBeAg at baseline, and 15 of the 16 patients seroconverted to anti-HBe during the observation period. T1762A1764 mutation was detected in 16 of 22 patients, including 11 patients positive for HBeAg, at baseline. During the follow-up period, A1896 mutation emerged in 7 of 16 patients who had the wild-type HBV or only the T1762A1764 mutation at baseline. Sustained remission of hepatitis correlated with the low level of viremia, but did not with type of mutations. These results indicate that HBV with T1762A1764 mutation tends to precede A1896 mutation during the course of infection in Japanese patients with chronic liver disease.</description><subject>Adult</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Hepatitis B Antibodies - blood</subject><subject>Hepatitis B e Antigens - blood</subject><subject>Hepatitis B virus - genetics</subject><subject>Hepatitis B, Chronic - virology</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Kruppel-Like Factor 6</subject><subject>Kruppel-Like Transcription Factors</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Polymerase Chain Reaction</subject><subject>Proto-Oncogene Proteins</subject><subject>Trans-Activators - blood</subject><subject>Trans-Activators - genetics</subject><subject>Viral diseases</subject><subject>Viral hepatitis</subject><issn>0163-2116</issn><issn>1573-2568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpd0M9PFTEQB_DGaOCBnr2ZRhNui9P2bX94exBADIkXPG-67ayUdLfPdhfy_gb_aSo8PXjqdPLJdPol5D2DUwZcfN58YQBtq7lmfC3lK7JirRINb6V-TVbAZK0Zk4fkqJR7ADCKyQNyyJhguuXrFfm9oTFNP5sZ80iHFGN6bJYttZONuxIKTQMtmION1KWMdJvTmKqtwNcLPjcL_lpwclhomOg3u7UTlkrtHHCaC3V3OU3B2Rh3FQzoZvS039E7_EPm-sgZfQh5KW_Jm8HGgu_25zH5cXlxe_61ufl-dX2-uWmcAD03ErwzEo1tfa_RI7ZgnJCDAsF975SC3hveusFwhV4zrbQaBPNghO0RrTgmJy9z62_q5mXuxlAcxlgXT0vpFCht1txU-PE_eJ-WXKMpHWdrwY3hUNGHPVr6EX23zWG0edf9zbiCT3tgS01hyHZyofxzRjOQXDwBInuM4A</recordid><startdate>20010301</startdate><enddate>20010301</enddate><creator>KAJIYA, Yuji</creator><creator>HAMASAKI, Keisuke</creator><creator>EGUCHI, Katsumi</creator><creator>NAKATA, Keisuke</creator><creator>MIYAZOE, Seiji</creator><creator>TAKEDA, Yoshio</creator><creator>HIGASHI, Shinichirou</creator><creator>OHKUBO, Kazuaki</creator><creator>ICHIKAWA, Tatsuki</creator><creator>NAKAO, Kazuhiko</creator><creator>KATO, Yuji</creator><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20010301</creationdate><title>A long-term follow-up analysis of serial core promoter and precore sequences in Japanese patients chronically infected by hepatitis B virus</title><author>KAJIYA, Yuji ; 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Sixteen of 22 patients were positive for HBeAg at baseline, and 15 of the 16 patients seroconverted to anti-HBe during the observation period. T1762A1764 mutation was detected in 16 of 22 patients, including 11 patients positive for HBeAg, at baseline. During the follow-up period, A1896 mutation emerged in 7 of 16 patients who had the wild-type HBV or only the T1762A1764 mutation at baseline. Sustained remission of hepatitis correlated with the low level of viremia, but did not with type of mutations. These results indicate that HBV with T1762A1764 mutation tends to precede A1896 mutation during the course of infection in Japanese patients with chronic liver disease.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>11318524</pmid><doi>10.1023/A:1005582812466</doi><tpages>7</tpages></addata></record> |
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| ispartof | Digestive diseases and sciences, 2001-03, Vol.46 (3), p.509-515 |
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| subjects | Adult Base Sequence Biological and medical sciences Female Follow-Up Studies Hepatitis B Antibodies - blood Hepatitis B e Antigens - blood Hepatitis B virus - genetics Hepatitis B, Chronic - virology Human viral diseases Humans Infectious diseases Kruppel-Like Factor 6 Kruppel-Like Transcription Factors Male Medical sciences Middle Aged Mutation Polymerase Chain Reaction Proto-Oncogene Proteins Trans-Activators - blood Trans-Activators - genetics Viral diseases Viral hepatitis |
| title | A long-term follow-up analysis of serial core promoter and precore sequences in Japanese patients chronically infected by hepatitis B virus |
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