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Article: Significance of viral load, core promoter/precore mutations and specific sequences of polymerase gene in HBV-infected patients on 3-year lamivudine treatment

TitleSignificance of viral load, core promoter/precore mutations and specific sequences of polymerase gene in HBV-infected patients on 3-year lamivudine treatment
Authors
Issue Date2006
PublisherInternational Medical Press. The Journal's web site is located at http://www.intmedpress.com/Journals/AVT/journals_avt_home.cfm
Citation
Antiviral Therapy, 2006, v. 11 n. 6, p. 779-786 How to Cite?
AbstractBackground: Comprehensive study on viral factors predicting treatment responsiveness to lamivudine is lacking. Aims: To define the significance of various viral factors and changes of viral population with lamivudine treatment. Patients and methods: Hepatitis B virus (HBV) DNA levels at baseline, week 24, 52 and year 3 were measured in 80 patients on continuous lamivudine therapy for 3 years. Genotypes, core promoter/precore mutations, YMDD mutations, polymorphic sequence of polymerase gene (rt91I/L, rt256S/C) were determined at baseline, week 12, 24 and 52. YMDD mutations were also determined at year 3. Results: High alanine aminotransferase levels and presence of core promoter/precore mutations at baseline were associated with higher chance of achieving HBV DNA <1,000 copies/ml (good response) and higher rate of hepatitis Be antigen (HBeAg) seroconversion at week 52. Achieving HBV DNA levels <1,000 copies/ml at week 24 as well as baseline core promoter/precore mutations were associated with higher chance of achieving good response, higher rate of HBeAg seroconversion and lower rate of YMDD mutations at year 3. Lamivudine reversed core promoter mutations to wild type in 25% of patients. All 5 patients with rt256C had poor HBV DNA response, persistent HBeAg and YMDD mutations by year 3. There was no difference in treatment response between patients with genotype B and C. Conclusions: Achieving HBV DNA levels <1,000 copies/ml at 24 week is the best target for short- and long-term treatment efficacy. Core promoter and precore mutations were associated with better treatment outcome, and rt256C polymorphism in the polymerase gene with poor response. © 2006 International Medical Press.
Persistent Identifierhttp://hdl.handle.net/10722/163031
ISSN
2023 Impact Factor: 1.3
2023 SCImago Journal Rankings: 0.447
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuen, MFen_US
dc.contributor.authorSablon, Een_US
dc.contributor.authorLibbrecht, Een_US
dc.contributor.authorVan De Velde, Hen_US
dc.contributor.authorWong, DKHen_US
dc.contributor.authorFung, Jen_US
dc.contributor.authorWong, BCYen_US
dc.contributor.authorLai, CLen_US
dc.date.accessioned2012-09-05T05:26:48Z-
dc.date.available2012-09-05T05:26:48Z-
dc.date.issued2006en_US
dc.identifier.citationAntiviral Therapy, 2006, v. 11 n. 6, p. 779-786en_US
dc.identifier.issn1359-6535en_US
dc.identifier.urihttp://hdl.handle.net/10722/163031-
dc.description.abstractBackground: Comprehensive study on viral factors predicting treatment responsiveness to lamivudine is lacking. Aims: To define the significance of various viral factors and changes of viral population with lamivudine treatment. Patients and methods: Hepatitis B virus (HBV) DNA levels at baseline, week 24, 52 and year 3 were measured in 80 patients on continuous lamivudine therapy for 3 years. Genotypes, core promoter/precore mutations, YMDD mutations, polymorphic sequence of polymerase gene (rt91I/L, rt256S/C) were determined at baseline, week 12, 24 and 52. YMDD mutations were also determined at year 3. Results: High alanine aminotransferase levels and presence of core promoter/precore mutations at baseline were associated with higher chance of achieving HBV DNA <1,000 copies/ml (good response) and higher rate of hepatitis Be antigen (HBeAg) seroconversion at week 52. Achieving HBV DNA levels <1,000 copies/ml at week 24 as well as baseline core promoter/precore mutations were associated with higher chance of achieving good response, higher rate of HBeAg seroconversion and lower rate of YMDD mutations at year 3. Lamivudine reversed core promoter mutations to wild type in 25% of patients. All 5 patients with rt256C had poor HBV DNA response, persistent HBeAg and YMDD mutations by year 3. There was no difference in treatment response between patients with genotype B and C. Conclusions: Achieving HBV DNA levels <1,000 copies/ml at 24 week is the best target for short- and long-term treatment efficacy. Core promoter and precore mutations were associated with better treatment outcome, and rt256C polymorphism in the polymerase gene with poor response. © 2006 International Medical Press.en_US
dc.languageengen_US
dc.publisherInternational Medical Press. The Journal's web site is located at http://www.intmedpress.com/Journals/AVT/journals_avt_home.cfmen_US
dc.relation.ispartofAntiviral Therapyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAlanine Transaminase - Blooden_US
dc.subject.meshAntiviral Agents - Therapeutic Useen_US
dc.subject.meshDna, Viral - Blooden_US
dc.subject.meshDna-Directed Dna Polymerase - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshHepatitis B Core Antigens - Geneticsen_US
dc.subject.meshHepatitis B Virus - Drug Effects - Enzymology - Geneticsen_US
dc.subject.meshHepatitis B, Chronic - Drug Therapy - Virologyen_US
dc.subject.meshHumansen_US
dc.subject.meshLamivudine - Therapeutic Useen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMutationen_US
dc.subject.meshPolymorphism, Geneticen_US
dc.subject.meshPromoter Regions, Genetic - Geneticsen_US
dc.subject.meshProtein Precursors - Geneticsen_US
dc.subject.meshReverse Transcriptase Inhibitors - Therapeutic Useen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTreatment Outcomeen_US
dc.subject.meshViral Loaden_US
dc.titleSignificance of viral load, core promoter/precore mutations and specific sequences of polymerase gene in HBV-infected patients on 3-year lamivudine treatmenten_US
dc.typeArticleen_US
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_US
dc.identifier.emailWong, DKH:danywong@hku.hken_US
dc.identifier.emailFung, J:jfung@sicklehut.comen_US
dc.identifier.emailWong, BCY:bcywong@hku.hken_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.authorityYuen, MF=rp00479en_US
dc.identifier.authorityWong, DKH=rp00492en_US
dc.identifier.authorityFung, J=rp00518en_US
dc.identifier.authorityWong, BCY=rp00429en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid17310822-
dc.identifier.scopuseid_2-s2.0-33749324215en_US
dc.identifier.hkuros130675-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33749324215&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume11en_US
dc.identifier.issue6en_US
dc.identifier.spage779en_US
dc.identifier.epage786en_US
dc.identifier.isiWOS:000240902200012-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridYuen, MF=7102031955en_US
dc.identifier.scopusauthoridSablon, E=6603694538en_US
dc.identifier.scopusauthoridLibbrecht, E=14825264600en_US
dc.identifier.scopusauthoridVan De Velde, H=36883501800en_US
dc.identifier.scopusauthoridWong, DKH=7401535819en_US
dc.identifier.scopusauthoridFung, J=23091109300en_US
dc.identifier.scopusauthoridWong, BCY=7402023340en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US
dc.identifier.issnl1359-6535-

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