Abstract: Baseline samples (n = 105) from adefovir refractory patients were tested for the presence of rtN236T using a highly sensitive allele-specific PCR assay with an rtN236T detection cut-off of 0.5%.
Abstract: Despite low levels of cross-resistance in vitro, TDF similarly suppresses wild-type and rtN236T mutant viruses in vivo.
Abstract: In conclusion, the rtN236T mutant virus showed similar HBV DNA decline kinetics to wild-type virus in adefovir refractory patients who switched to TDF or FTC/TDF.
Abstract: In patients with rtN236T, wild-type and rtN236T
Hepatitis B e antigen-suppressing mutations enhance the replication efficiency of adefovir-resistant hepatitis B virus strains.
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+
HBV mutation literature information.
PMID: 
2013
Journal of viral hepatitis
Browser Board
Co-occurred Entities
Filtrator
ViMRT