Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.antiviral.2005.11.005
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dc.titleAre in vitro hepatitis B core promoter mutations important for clinical alterations in viral load?
dc.contributor.authorCheng, Y.
dc.contributor.authorSeet, B.L.
dc.contributor.authorOng, C.S.L.
dc.contributor.authorWasser, S.
dc.contributor.authorLim, S.G.
dc.contributor.authorTan, T.M.C.
dc.contributor.authorPeter, F.J.
dc.date.accessioned2011-09-27T05:44:45Z
dc.date.available2011-09-27T05:44:45Z
dc.date.issued2006
dc.identifier.citationCheng, Y., Seet, B.L., Ong, C.S.L., Wasser, S., Lim, S.G., Tan, T.M.C., Peter, F.J. (2006). Are in vitro hepatitis B core promoter mutations important for clinical alterations in viral load?. Antiviral Research 69 (3) : 142-151. ScholarBank@NUS Repository. https://doi.org/10.1016/j.antiviral.2005.11.005
dc.identifier.issn01663542
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/27102
dc.description.abstractIn vitro studies of HBV core promoter mutations in hepatoma cell lines suggest that some mutations in core promoter transcription factor binding sites result in reduced core promoter activity and viral replication. We sought to validate this hypothesis using clinical samples with viral load differences before and after HBeAg seroconversion. A consensus sequence for transcription factor binding sites/regulatory regions was constructed based on published studies. Serum from two time points in 33 seroconverters and 10 interferon non-responders (controls) were utilized. Genotyping, HBV DNA quantification and direct sequencing of core promoter were performed. There were 216 new mutations following HBeAg seroconversion but few in controls. Mutations or mismatches to consensus transcription factor/regulatory region sequences clustered at nucleotide positions appeared genotype-specific, non-group specific or baseline mismatches and were discounted as having significant impact on viral replication. Only a few mutations in three seroconverters (9.1%) were specific, while 39.4% had no new mutations that could be attributed to reduction in viral load following HBeAg seroconversion. In 51.5% of patients, mutations were of uncertain significance because they occurred in demonstrated non-critical clustered nucleotide positions. Core promoter mutations post-seroconversion did not correlate with in vitro induced mutations that reduced the promoter activity. © 2005 Elsevier B.V. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.antiviral.2005.11.005
dc.sourceScopus
dc.subjectCore promoter
dc.subjectHepatitis B e antigen seroconversion
dc.subjectHepatitis B virus
dc.subjectMutation
dc.subjectTranscription factors
dc.typeArticle
dc.contributor.departmentOFFICE OF LIFE SCIENCES
dc.contributor.departmentMEDICINE
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.1016/j.antiviral.2005.11.005
dc.description.sourcetitleAntiviral Research
dc.description.volume69
dc.description.issue3
dc.description.page142-151
dc.identifier.isiut000236084800002
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