Result: Besides, another ADV-associated resistant mutation rtN236T had a higher prevalence in genotype B than genotype C in ADV-resistant patients (66.7% vs.
Result: The rate of other drug-associated resistant mutation models, such as rtA181T+rtN236T for ADV, rtL180M+rtM204V+rtS202G for ETV, and rtL180M+rtM204V+rtT184L for ETV, did not differ between genotypes
Investigation into drug-resistant mutations of HBV from 845 nucleoside/nucleotide analogue-naive Chinese patients with chronic HBV infection.
Abstract: Phenotypic analysis of patient-derived viral strains showed that rtA181S, rtA181S+N236T, rtN236T and rtA181V strains had 68.5%, 49.9%, 71.4% and 66.2% of natural replication capacity of wild-type strain, and 3.7-fold, 9.8-fold, 7.9-fold and 5.6-fold increased EC(50) to adefovir dipivoxil (ADV).
Long-term outcomes and dynamics of mutants associated with lamivudine-adefovir rescue therapy in patients with lamivudine-resistant chronic hepatitis B.
Result: LAM-resistant (rtL180M and rtM204I/V) and ADV-resistant (rtA181V/T and rtN236T) mutation profiles were followed through RFMP assay at weeks 48 and 96 of the combination therapy.
Result: The ADV-resistant mutation, rtN236T was not found in 12 patients at 48 and 96 weeks of rescue therapy; however, rtA181T mutants emerged as a minor population in two and four patients at weeks 48 and 96, respectively.
[Clinical emergence features and implications of hepatitis B virus rtA181T mutation].
Abstract: RESULTS: The incidence of rtA181T across the study population was 4.1% (165/3, 013), and most of the rtAl 81T-positive patients had received adefovir and/or lamivudine.Forty percent (66/165) of the rtA 181T cases were single mutants and treatment responsive, 46.1% (76/165) included the adefovir-resistant mutation rtA 181 V/N236T, 12.1% (20/165) included the lamivudine-resistant mutation rtM204V/rtM2041, and 1.8% (3/165) included multidrug-resistant mutations.Interestingly, 73.9% (122/165) of the rtA181T-positive samples were detected with co-existing wild-type nucleotides at the site.
Microarray-based genotyping and detection of drug-resistant HBV mutations from 620 Chinese patients with chronic HBV infection.
PMID: 25982306
2015
The Brazilian journal of infectious diseases
Abstract: Of these, nine and eight patients carried lamivudine (LAM)-/telbivudine (LdT)-resistance mutations (rtL180M, rtM204I/V) and adefovir (ADV)-resistance mutations (rtA181T/V, rtN236T), respectively.
Delayed Reduction of Hepatitis B Viral Load and Dynamics of Adefovir-Resistant Variants during Adefovir plus Entecavir Combination Rescue Therapy.
PMID: 26005376
2015
International journal of medical sciences
Abstract: RESULTS: HBV DNA decreased to the lowest level during ADV monotherapy at 6-18 months, with a decrease of 0.95-5.51 log10 copies/mL, whereas rtA181V or rtN236T gradually increased with extended therapy.
Abstract: Resistant rtA181V and rtN236T were undetectable after 21-24 months of combination therapy.
Introduction: They include rtA181V/T and rtN236T.
Discussion: In contrast, in the present study, we observed that replication of the ADV-resistant variants, rtA181V and/
A novel pyridazinone derivative inhibits hepatitis B virus replication by inducing genome-free capsid formation.
PMID: 26349829
2015
Antimicrobial agents and chemotherapy
Abstract: Both the 3TC/ETV dually resistant L180M/M204I mutant and the adefovir (ADV)-resistant A181T/N236T mutant were as susceptible to 3711 as wild-type HBV.
Mechanism of Adefovir, Tenofovir and Entecavir Resistance: Molecular Modeling Studies of How A Novel Anti-HBV Agent (FMCA) Can Overcome the Drug Resistance.
Abstract: In this regard, homology modeled structure of HBV polymerase was used for minimization, conformational search and Glide XP docking followed by binding energy calculation on wild-type as well as on mutant HBV-polymerases (N236T, L180M+M204V+S202G & A194T).
4'-modified nucleoside analogs: potent inhibitors active against entecavir-resistant hepatitis B virus.
Result: CAdA and CdG block HBVETV-RL180M/S202G/M204V and HBVADV-RA181T/N236T replication.
Result: S2, both CAdA and CdG were active against HBVADV-RA181T/N236T with IC50s of 0.09 and 0.04 muM, respectively, although ADV had a significantly greater IC50 value of 39.5 muM.
Result: We also determined the activity of CAdA and CdG against HBVADV-RA181T/N236T.
Result: We subsequently asked whether CAdA and CdG blocked the replication of ETV-resistant HBV (HBVETV-RL180M/S202G/M204V) and ADV-resistant HBV (HBVADV-RA181T/N236T).
HBV mutation literature information.
PMID: 
2015
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