Result: There were no drug resistant mutations (lamivudine-resistant pattern: rtM204V/I, rtL180M, rtV173L, adefovir-resistant pattern: rtA181V/T, tenofovir-resistant pattern: rtA194T and entecavir-resistant pattern: rtL180M, rtS202G, rtM204V) detectable in acute patients belonging to our study population.
Epidemiology study of HBV genotypes and antiviral drug resistance in multi-ethnic regions from Western China.
Result: Nevertheless, LMV-associated mutation rtM204V/I and rtL180M, LdT-associated mutation rtM204I, and ETV-associated mutations rtT184A/I/S, rtS202G and rtM250L didn't differ significantly between genotype B and C (P > 0.05).
Result: The rate of other drug-associated resistant mutation models, such as rtA181T+rtN236T for ADV, rtL180M+
Analysis of HBV genotype, drug resistant mutations, and pre-core/basal core promoter mutations in Korean patients with acute hepatitis B.
Abstract: No patient showed mutations that conferred resistance against lamivudine (L180M, M204V/I), adefovir (A181T, N236S), or entecavir (I169M, A184T/V, S202I/G, M250V/I/L).
Virologic breakthrough in a patient with chronic hepatitis B by combination treatment with tenofovir disoproxil fumarate and entecavir.
PMID: 25061278
2014
Drug design, development and therapy
Abstract: Amino acid substitutions of rtL180M, rtS202G, and rtM204V emerged and were associated with an increase in serum HBV DNA at virologic breakthrough.
Conclusion: In comparison with those at the start of TDF therapy, the amino acid substitutions changed from rtL180M, rtT184M, and rtM204V to rtL180M, rtS202G, and rtM204V, and no other amino acid substitut
Adefovir and lamivudine combination therapy in patients with entecavir-resistant chronic hepatitis B: antiviral responses and evolution of mutations.
Result: It is worth noting that we did not observe any of the common NA-related resistance mutations including rtM204V/I, rtS202C/G/I, rtL180M, rtA181T/V, rtT184A/I/L/G/C/M, rtA194T, rtI169T, rtV173L, rtL80I, rtN236T, and
PMID: 24697270
2014
The Journal of organic chemistry
Abstract: FMCA demonstrated excellent anti-HBV activity against both adefovir-resistant and lamivudine-resistant double (rtL180M/rtM204V) mutants as well as in lamivudine/entecavir triple mutants (L180M+S202G+M204V) in vitro.
[Investigation of baseline antiviral resistance in treatment-naive chronic hepatitis B cases].
Abstract: Mutations conferring resistance to entecavir + lamivudine (S202G, M204V, L180M, T184N) were identified in one patient whereas L180P, A181Q and A194V substitutions associated with probable lamivudin + adefovir and tenofovir resistance, respectively, were detected in other patients.
[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.
Quasispecies and pre-existing drug-resistant mutations of hepatitis B virus in patients with chronic hepatitis B.
Abstract: In patient 3, mutations conferring resistance to adefovir at V84I (5%), I169L (1%), and N236H<
Discussion: The LAM resistance quasispecies (rtM204V+-rt180M) emerged as early as 48 weeks, and ETV resistant quasispecies (rtM204+-rtL180M plus S202G) were found after 112 weeks.
Discussion: Unlike the previous study, rtI169S/L and/or rtS202G mutations were detected in the absence of LAM resistance variants at pretreatment, even though those variants disappeared during LAM therapy until VB.
HBV mutation literature information.
PMID: 
2015
PloS one
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