{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T17:15:52Z","timestamp":1791393352256,"version":"4.3.3"},"reference-count":42,"publisher":"Microbiology Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,9,1]]},"abstract":"<jats:p>To investigate the role of pre-core and basal core promoter (BCP) mutants in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (e-CHB) in Iran, <jats:italic>Hepatitis B virus<\/jats:italic> strains from 30 patients and 42 anti-HBe-positive asymptomatic carriers (ASCs) were characterized. G<jats:sup>1896<\/jats:sup>A pre-core stop mutants, detected in 77\u200a% of e-CHB patients and 85\u200a% of ASCs, showed no association with virus load or aminotransferase levels. Twenty per cent of e-CHB patients and 31\u200a% of ASCs harboured T<jats:sup>1762<\/jats:sup>A<jats:sup>1764<\/jats:sup> mutants. When this double mutation was associated with G<jats:sup>1757<\/jats:sup>, it was linked to a higher virus load in patients than when it was associated with A<jats:sup>1757<\/jats:sup> (10<jats:sup>5\u00b72\u00b11\u00b78<\/jats:sup> vs 10<jats:sup>3\u00b72\u00b10\u00b78<\/jats:sup>\u2005copies\u2005ml<jats:sup>\u22121<\/jats:sup>; <jats:italic>P<\/jats:italic>=0\u00b7004). Interestingly, the most common BCP mutations were T<jats:sup>1764<\/jats:sup> and G<jats:sup>1766<\/jats:sup>, which were present in 33\u200a% of e-CHB patients and 29\u200a% of ASCs. These were associated with higher virus load and aminotransferase levels compared with patients lacking core promoter mutations, although this was not significant. The T<jats:sup>1764<\/jats:sup>G<jats:sup>1766<\/jats:sup> double mutation was only present in strains with A<jats:sup>1757<\/jats:sup> (<jats:italic>P<\/jats:italic>&lt;0\u00b7001), which is more frequent in strains of genotype D than in those belonging to other genotypes. On the other hand, the T<jats:sup>1762<\/jats:sup>A<jats:sup>1764<\/jats:sup> double mutation was found more frequently in association with G<jats:sup>1757<\/jats:sup> than with A<jats:sup>1757<\/jats:sup>. The T<jats:sup>1762<\/jats:sup>A<jats:sup>1764<\/jats:sup> double mutation forms a binding site for hepatocyte nuclear factor 1 (HNF1), which is constrained by A<jats:sup>1757<\/jats:sup>. However, the T<jats:sup>1764<\/jats:sup>G<jats:sup>1766<\/jats:sup> double mutant may form a binding site for HNF3. Thus, position 1757 affects the emergence of promoter double mutants and would predict a relative genotypic restriction of both the T<jats:sup>1762<\/jats:sup>A<jats:sup>1764<\/jats:sup> and the T<jats:sup>1764<\/jats:sup>G<jats:sup>1766<\/jats:sup> double mutants.<\/jats:p>","DOI":"10.1099\/vir.0.81023-0","type":"journal-article","created":{"date-parts":[[2005,8,12]],"date-time":"2005-08-12T00:40:29Z","timestamp":1123807229000},"page":"2451-2458","source":"Crossref","is-referenced-by-count":32,"title":["T1764G1766 core promoter double mutants are restricted to Hepatitis B virus strains with an A1757 and are common in genotype D"],"prefix":"10.1099","volume":"86","author":[{"given":"Hossein","family":"Sendi","sequence":"first","affiliation":[{"name":"Research Center for Gastroenterology and Liver Diseases, Shaheed Beheshti University of Medical Sciences, Taleghani Hospital, Tabnak Avenue, 19857 Tehran, Iran"},{"name":"Microbiology and Tumor Biology Center, Karolinska Institutet, SE-171 77 Stockholm, Sweden"},{"name":"Department of Virology, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marjan","family":"Mehrab-Mohseni","sequence":"additional","affiliation":[{"name":"Research Center for Gastroenterology and Liver Diseases, Shaheed Beheshti University of Medical Sciences, Taleghani Hospital, Tabnak Avenue, 19857 Tehran, Iran"},{"name":"Department of Virology, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammad R.","family":"Zali","sequence":"additional","affiliation":[{"name":"Research Center for Gastroenterology and Liver Diseases, Shaheed Beheshti University of Medical Sciences, Taleghani Hospital, Tabnak Avenue, 19857 Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helene","family":"Norder","sequence":"additional","affiliation":[{"name":"Microbiology and Tumor Biology Center, Karolinska Institutet, SE-171 77 Stockholm, Sweden"},{"name":"Department of Virology, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars O.","family":"Magnius","sequence":"additional","affiliation":[{"name":"Microbiology and Tumor Biology Center, Karolinska Institutet, SE-171 77 Stockholm, Sweden"},{"name":"Department of Virology, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"345","reference":[{"key":"R1","doi-asserted-by":"crossref","first-page":"227","DOI":"10.1002\/jmv.20261","article-title":"Genotype characterization and phylogenetic analysis of hepatitis B virus isolates from Iranian patients","volume":"75","author":"Amini-Bavil-Olyaee","year":"2005","journal-title":"J Med 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