{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T17:42:16Z","timestamp":1775151736912,"version":"3.50.1"},"reference-count":46,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,2,24]],"date-time":"2005-02-24T00:00:00Z","timestamp":1109203200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2005,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background:<\/jats:bold> The clinicopathological profiles and outcome of chronic hepatitis B can differ by hepatitis B virus (HBV) genotypes. In Japan, genotype B and C are two major HBV genotypes. The basic core promoter and precore mutations are other known viral factors for disease activity, although the relationship between HBV genotypes and these mutations is not fully understood.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> The HBV genotypes in 90 patients with chronic hepatitis B were determined using an ELISA. Obtained data were correlated with clinicopathological parameters, basic core promoter, precore and the nucleotide 1858 mutations of the HBV genome.<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> Among 90 cases, 20 (22.2%) had genotype B and 70 (77.8%) had genotype C HBV. Genotype B patients were older than genotype C patients (44.0\u2003\u00b1\u200313.9 vs 34.7\u2003\u00b1\u200311.0 <jats:italic>P<\/jats:italic>\u2003=\u20030.0022). The HBeAg was more prevalent in genotype C than B patients (<jats:italic>P\u2003=<\/jats:italic>\u20030.0008) while anti\u2010HBe was more common in genotype B than C patients (<jats:italic>P\u2003=<\/jats:italic>\u20030.0002). Serum aspartate aspartate aminotransferase\/alanine aminotransferase levels (B: 220.7\u2003\u00b1\u2003612.8\/257.0\u2003\u00b1\u2003498.0\u2003IU\/L vs C: 111.3\u2003\u00b1\u2003122.8\/201.6\u2003\u00b1\u2003229.4\u2003IU\/L, <jats:italic>P<\/jats:italic>\u2003=\u20030.16\/0.48) and HBV viral loads in blood (B: 6.1\u2003\u00b1\u20033.1\u2003log genome equivalent [LGE]\/mL vs C: 6.7\u2003\u00b1\u20032.3\u2003LGE\/mL, <jats:italic>P<\/jats:italic>\u2003=\u20030.42) were equivalent. The seroconversion from HBeAg to anti\u2010HBe occurred significantly earlier in genotype B than C patients (62\u2003\u00b1\u200353\u2003months vs 136\u2003\u00b1\u200354\u2003months, <jats:italic>P<\/jats:italic>\u2003=\u20030.0028) during the mean observation period of 149\u2003\u00b1\u200382\u2003months even under various therapeutic modalities. The categories III and IV of the histological activity index in genotype C were higher (III: <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.005, IV: <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.05, <jats:italic>n<\/jats:italic>\u2003=\u200368) than that in B patients whereas category II was higher in genotype B than C patients (<jats:italic>P\u2003&lt;<\/jats:italic>\u20030.05). The double mutation (1762T\/1764A) in the basic core promoter was more frequently found in genotype C than in B HBV (<jats:italic>P<\/jats:italic>\u2003=\u20030.0068), whereas the precore mutation (1896A) was more common in genotype B than C HBV (<jats:italic>P<\/jats:italic>\u2003=\u20030.0233). The incidence of 1858C that was complementary to the precore mutation site in the stem\u2010loop structure \u2208, was equally rare in both genotype B and C HBV.<\/jats:p><jats:p><jats:bold>Conclusions:<\/jats:bold> Genotype B patients were older, had earlier HBeAg seroconversion and exhibited more severe lobular necroinflammation, less portal inflammation and fibrosis than genotype C patients. This genotypic difference is related to the basic core promoter and precore mutations irrespective of 1858C.<\/jats:p><jats:p>\u00a9 2004 Blackwell Publishing Asia Pty Ltd<\/jats:p>","DOI":"10.1111\/j.1440-1746.2004.03572.x","type":"journal-article","created":{"date-parts":[[2005,2,24]],"date-time":"2005-02-24T10:14:56Z","timestamp":1109240096000},"page":"441-449","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Comparative study of genotype B and C hepatitis B virus\u2010induced chronic hepatitis in relation to the basic core promoter and precore mutations"],"prefix":"10.1111","volume":"20","author":[{"given":"KOJI","family":"WATANABE","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"TORU","family":"TAKAHASHI","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"SUMIO","family":"TAKAHASHI","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"SHOGO","family":"OKOSHI","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"TAKAFUMI","family":"ICHIDA","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"YUTAKA","family":"AOYAGI","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,2,24]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197604012941402"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1159\/000171343"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(91)90296-W"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/hep.510270137"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1572-0241.2000.03201.x"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(91)90286-T"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199106133242404"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199106133242405"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1006\/viro.1993.1257"},{"key":"e_1_2_6_11_2","doi-asserted-by":"crossref","first-page":"6785","DOI":"10.1128\/JVI.72.8.6785-6795.1998","article-title":"Naturally occurring mutations define a novel function of the hepatitis B virus core promoter in core protein expression","volume":"72","author":"Baumert TF","year":"1998","journal-title":"J. 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