Abstract: All rtN236T- or rtA181V/T-containing constructs, regardless of concomitant PC or BCP mutations, were resistant to adefovir, but remained susceptible to telbivudine, entecavir and tenofovir.
Abstract: The adefovir-resistant polymerase mutations rtN236T, rtA181V and rtA181T showed a drastically reduced viral replication compared with WT.
Abstract: Therefore, HBV constructs with wild type (WT) or adefovir-resistant rtN236T,
Characterization of antiviral resistance mutations among the Eastern Indian Hepatitis B virus infected population.
Introduction: The primary adefovir-resistant mutations significantly associated with treatment failure are rtN236T and rtA181T/V .
Detection of rtN236T mutation associated with adefovir dipivoxil resistance in Hepatitis B infected patients with YMDD mutations in Tehran.
PMID: 23467016
2013
Iranian journal of microbiology
Abstract: RESULTS: After alignment of protein coding sequences, the rtN236T mutation was observed in two (6.6%) patients, while twenty-eight others had neither rtN236T, nor rtA181V/T mutation.
Abstract: The mutations known as causing adefovir resistance, rtN236T and rtA181V/T, are detected within the D and B functional domain of the HBV polymerase, respectively.
Result: After alignment of protein coding sequences, the rtN236T mutation was observed in two (6.6%) patients.
Result: while twenty eight others had
Epidemiological, virological and clinical characteristics of HBV infection in 223 HIV co-infected patients: a French multi-centre collaborative study.
Result: rtV173L, rtL180M, rtA181V/T, rtT184G, rtS202I, rtM204V/I, rtN236T and rtM250V were first studied and then, others residues with changes present in at least two patients were further considered.
Drug-related mutational patterns in hepatitis B virus (HBV) reverse transcriptase proteins from Iranian treatment-naive chronic HBV patients.
Discussion: Adefovir resistance has been associated with a primary mutation in the D domain at rtN236T and rtA181T/Vin the B domain.
Discussion: These secondary mutations have also been detected in the absence of rtN236T (both alone and in combination) in patients who have either not responded to or have had a virological breakthrough during adefovir treatment.
Ultrasensitive amplification refractory mutation system real-time PCR (ARMS RT-PCR) assay for detection of minority hepatitis B virus-resistant strains in the era of personalized medicine.
PMID: 23804383
2013
Journal of clinical microbiology
Abstract: The assay showed 100% sensitivity for the detection of mutant variants A181V, T184A, and N236T in samples from 41 chronically HBV-infected patients under antiviral therapy who had developed resistance-associated mutations detected by direct PCR Sanger sequencing.
Substitution rtq267h of hepatitis B virus increases the weight of replication and Lamivudine resistance.
Introduction: Substitution rtA181V/T and/or rtN236T can reduce the anti-HBV effect of ADV, rtN238R, rtT240Y and rtN248H of HBV were newly reported to decrease susceptibility to ADV (8).
Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B.
Introduction: According to previously studies, the patterns of genotypic resistance in the HBV polymerase can be categorized into five specific evolutionary pathways, including L-nucleoside pathway (rtM204I [or V or I/V]), the acyclic phosphonate pathway (rtN236T), the shared pathway (rtA181T [or V or T/V]) of both L-nucleoside and acyclic phosphonate, ETV resistance pathway (rtL180M+rtM204V with one of either rtT184, S202 or M250 residue changes) and multidrug resistance pathways (rtA181T+
[Detection of resistance mutations in chronic hepatitis B patients receiving antiviral therapy for over one year].
Abstract: In one sample which had multiple mutations associated with LVD resistance single mutations (S202G, N236T) associated with entecavir resistance and in two other such samples mutations associated with adefovir resistance were detected by SEQ.
HBV mutation literature information.
PMID: 
2013
Journal of viral hepatitis
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