A novel mutation pattern emerging during lamivudine treatment shows cross-resistance to adefovir dipivoxil treatment

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dc.contributor.authorKaratayli, Ersin
dc.contributor.authorKarayalcin, Selim
dc.contributor.authorKaraaslan, Hayri
dc.contributor.authorKayhan, Handan
dc.contributor.authorTurkyilmaz, A. Resat
dc.contributor.authorSahin, Fikret
dc.contributor.authorYurdaydin, Cihan
dc.date.accessioned2020-03-26T17:16:57Z
dc.date.available2020-03-26T17:16:57Z
dc.date.issued2007
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractAims: This study was conducted to clarify the resistance profile of a novel mutation pattern emerging during lamivudine (3TC) therapy and showing cross-resistance to adefovir dipivoxil (ADV) in a patient with chronic hepatitis B. Methods and results: Successful suppression of hepatitis B virus (HBV) replication by sequential therapy of 9 MU thrice weekly interferon (IFN) and 3TC was followed by genotypical resistance detected at month 28 of therapy (month 19 of lamivudine treatment). ADV was added to 3TC therapy on month 44 of antiviral treatment. Neither alanine aminotransferase normalization nor a stable decrease in HBV viral load was observed, although ADV was used for more than 40 months. The HBV pol region was amplified from serum samples obtained before and after ADV treatment. The complete genome was cloned into a TA vector. PCR products and 7-10 clones from each cloned vector were sequenced. A novel mutation, A181S, in the reverse transcriptase gene leading to a conversion of W172C in the overlapping surface antigen gene was detected along with a M204I mutation. The complete genome comprising the A181S + M204I pattern was cloned into an expression vector and its in vitro susceptibility to 3TC, ADV, tenofovir (PMPA), clevudine (L-FMAU) and emtricitabine (FTC) were determined in transiently transfected Huh7 cells. This mutation pattern displayed more than 1,000-fold resistance to the nucleoside analogues 3TC and FTC and approximately sixfold resistance to L-FMAU, while it confers 28.23- and 5.57-fold resistance for the nucleotide analogues ADV and PMPA, respectively. Conclusion: A new mutation pattern, A181S + M204I, arising under lamivudine treatment confers cross-resistance to ADV both in vivo and in vitro.en_US
dc.identifier.endpage768en_US
dc.identifier.issn1359-6535en_US
dc.identifier.issue5en_US
dc.identifier.pmid17713159en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage761en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12395/21188
dc.identifier.volume12en_US
dc.identifier.wosWOS:000248546900007en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherINT MEDICAL PRESS LTDen_US
dc.relation.ispartofANTIVIRAL THERAPYen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.selcuk20240510_oaigen_US
dc.titleA novel mutation pattern emerging during lamivudine treatment shows cross-resistance to adefovir dipivoxil treatmenten_US
dc.typeArticleen_US

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