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Article: Evolution of primary and compensatory lamivudine resistance mutations in chronic hepatitis B virus-infected patients during long-term lamivudine treatment, assessed by a line probe assay

TitleEvolution of primary and compensatory lamivudine resistance mutations in chronic hepatitis B virus-infected patients during long-term lamivudine treatment, assessed by a line probe assay
Authors
Issue Date2007
Citation
Journal Of Clinical Microbiology, 2007, v. 45 n. 12, p. 3935-3941 How to Cite?
AbstractWith the availability of more potent nucleotide/nucleoside analogues, the early detection of drug-resistant mutants of hepatitis B virus (HBV) is important for the strategic treatment of chronic hepatitis B. We studied 336 serum samples from 80 patients chronically infected with HBV who were receiving lamivudine treatment for the presence of lamivudine resistance mutations at codons 80, 173, 180, and 204 of the HBV polymerase. The sequencing data were compared with the results generated with the INNO-LiPA HBV DR (drug resistance) v2 strip, a line probe assay (LiPA) covering wild-type and mutant motifs, for resistance mutations to lamivudine and adefovir dipivoxil. This method provided at least the same information as sequencing for 99.1% of all codons analyzed. On the basis of the LiPA results, 20 of 80 patients developed a lamivudine resistance mutation after 1 year. In all 20 patients, the mutation occurred in the YMDD motif at reverse transcriptase position 204 (rt204; M204V/I) either with or without the compensatory mutation at position rtl80 (L180M). A compensatory mutation at position rt80 (L80V/I) was detected in half of these patients. After 36 months, a compensatory mutation was seen at position rt173 (V173L) in 3/15 patients. Time-to-event survival analysis indicated a 2.8 times greater chance for LiPA to detect a given mutation than sequencing at any moment in time (hazard ratio, 2.8, 95% confidence interval, 1.79, 4.41; P < 0.0001). These results demonstrate that a highly sensitive and specific assay such as the INNO-LiPA HBV DR v2 can precociously detect and monitor the emergence of primary and compensatory lamivudine resistance mutations in patients chronically infected with HBV and is more sensitive than sequencing. Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/163133
ISSN
2015 Impact Factor: 3.631
2015 SCImago Journal Rankings: 2.151
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLibbrecht, Een_US
dc.contributor.authorDoutreloigne, Jen_US
dc.contributor.authorVan De Velde, Hen_US
dc.contributor.authorYuen, MFen_US
dc.contributor.authorLai, CLen_US
dc.contributor.authorShapiro, Fen_US
dc.contributor.authorSablon, Een_US
dc.date.accessioned2012-09-05T05:28:00Z-
dc.date.available2012-09-05T05:28:00Z-
dc.date.issued2007en_US
dc.identifier.citationJournal Of Clinical Microbiology, 2007, v. 45 n. 12, p. 3935-3941en_US
dc.identifier.issn0095-1137en_US
dc.identifier.urihttp://hdl.handle.net/10722/163133-
dc.description.abstractWith the availability of more potent nucleotide/nucleoside analogues, the early detection of drug-resistant mutants of hepatitis B virus (HBV) is important for the strategic treatment of chronic hepatitis B. We studied 336 serum samples from 80 patients chronically infected with HBV who were receiving lamivudine treatment for the presence of lamivudine resistance mutations at codons 80, 173, 180, and 204 of the HBV polymerase. The sequencing data were compared with the results generated with the INNO-LiPA HBV DR (drug resistance) v2 strip, a line probe assay (LiPA) covering wild-type and mutant motifs, for resistance mutations to lamivudine and adefovir dipivoxil. This method provided at least the same information as sequencing for 99.1% of all codons analyzed. On the basis of the LiPA results, 20 of 80 patients developed a lamivudine resistance mutation after 1 year. In all 20 patients, the mutation occurred in the YMDD motif at reverse transcriptase position 204 (rt204; M204V/I) either with or without the compensatory mutation at position rtl80 (L180M). A compensatory mutation at position rt80 (L80V/I) was detected in half of these patients. After 36 months, a compensatory mutation was seen at position rt173 (V173L) in 3/15 patients. Time-to-event survival analysis indicated a 2.8 times greater chance for LiPA to detect a given mutation than sequencing at any moment in time (hazard ratio, 2.8, 95% confidence interval, 1.79, 4.41; P < 0.0001). These results demonstrate that a highly sensitive and specific assay such as the INNO-LiPA HBV DR v2 can precociously detect and monitor the emergence of primary and compensatory lamivudine resistance mutations in patients chronically infected with HBV and is more sensitive than sequencing. Copyright © 2007, American Society for Microbiology. All Rights Reserved.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Clinical Microbiologyen_US
dc.rightsJournal of Clinical Microbiology. Copyright © American Society for Microbiology.-
dc.subject.meshAdenine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshAmino Acid Substitutionen_US
dc.subject.meshDrug Resistance, Viral - Geneticsen_US
dc.subject.meshEvolution, Molecularen_US
dc.subject.meshGene Products, Pol - Geneticsen_US
dc.subject.meshHepatitis B Virus - Drug Effects - Geneticsen_US
dc.subject.meshHepatitis B, Chronic - Drug Therapy - Virologyen_US
dc.subject.meshHumansen_US
dc.subject.meshLamivudine - Therapeutic Useen_US
dc.subject.meshMutation, Missenseen_US
dc.subject.meshNucleic Acid Hybridization - Methodsen_US
dc.subject.meshPhosphonic Acids - Pharmacologyen_US
dc.subject.meshSequence Analysis, Dnaen_US
dc.subject.meshTime Factorsen_US
dc.titleEvolution of primary and compensatory lamivudine resistance mutations in chronic hepatitis B virus-infected patients during long-term lamivudine treatment, assessed by a line probe assayen_US
dc.typeArticleen_US
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.authorityYuen, MF=rp00479en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1128/JCM.00020-07en_US
dc.identifier.pmid17913933-
dc.identifier.pmcidPMC2168556-
dc.identifier.scopuseid_2-s2.0-37249029182en_US
dc.identifier.hkuros149099-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-37249029182&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume45en_US
dc.identifier.issue12en_US
dc.identifier.spage3935en_US
dc.identifier.epage3941en_US
dc.identifier.isiWOS:000251630000011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLibbrecht, E=14825264600en_US
dc.identifier.scopusauthoridDoutreloigne, J=6603727456en_US
dc.identifier.scopusauthoridVan De Velde, H=36883501800en_US
dc.identifier.scopusauthoridYuen, MF=7102031955en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US
dc.identifier.scopusauthoridShapiro, F=35863544900en_US
dc.identifier.scopusauthoridSablon, E=6603694538en_US
dc.customcontrol.immutablejt 130709-

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