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
Conclusion: Further, there were no substitutions that could be associated with reduced TDF susceptibility (rtA181V/T, rtN236T, or rtA194T) in April 2013.
Discussion: For these 45 patients, which included ten with virologic breakthrough, both line probe assay and direct sequencing revealed no new amino acid substitutions, including substitutions that could be associated with reduced TDF susceptibility (rtA181V/T, rtN236T, or rtA194T).
Long-term efficacy and emergence of multidrug resistance in patients with lamivudine-refractory chronic hepatitis B treated by combination therapy with adefovir plus lamivudine.
Abstract: HBV DNA levels of patients with rtA181S mutation at baseline and emergence of rtA181T + rtN236T double mutation or a wide variety of mutations during combination therapy could not be suppressed.
Abstract: Moreover, using ultra-deep sequencing, rtA181T/V mutations were detected at baseline in 7 of 10 patients with emergent multidrug resistance during combination therapy, although 6 of these 7 patients had very low frequency (<1 %) variants.
Resistant mutants induced by adefovir dipivoxil in hepatitis B virus isolates.
PMID: 25493022
2014
World journal of gastroenterology
Abstract: Patients with the rtA181T mutant were primarily infected with genotype C and e-antigen negative HBV, while patients with the rtN236T mutant were primarily infected by genotype B HBV (chi(2) = 6.004, 7.159; P = 0.023, 0.007).
Abstract: The most prevalent mutations were rtA181T, rtV214A, and rtN236T.
Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers.
PMID: 25320728
2014
Clinical and molecular hepatology
Discussion: In this regard, we previously found several point mutations in the MHR region and W172stop corresponding to the multidrug-resistant rtA181T mutation in polymerase impair the secretion of both virions and HBsAg.
Different mechanism of selection of adefovir-resistant mutant viruses during adefovir monotherapy in patients with lamivudine-resistant chronic hepatitis B.
Abstract: CONCLUSION: The high rate of ADV resistance in patients with LMV-resistance might be attributable to preexisting rtA181V/T mutant virus.
Abstract: During ADV therapy, most rtM204V/I mutants were replaced by wild type in all 3 patients without the rtA181V/T mutation and in one patient with the rtA181V/T mutation.
Abstract: In patients with the rtA181V/T mutation (n = 6), the rtA181V/T mutant overtook the rtM204V/I mutant in 3 of 4 patients wi
Molecular epidemiology and genotyping of hepatitis B virus of HBsAg-positive patients in Oman.
Discussion: Besides other previously described resistance mutations, the best-described drug resistance mutations are the LAM resistance mutations rtL180M and rtM204V/I and the adefovir resistance mutations rtA181V/T and rtN236T.
Discussion: Other antiviral therapy resistance mutations, such as rtA181V/T or rtN236T, were not detected.
Novel natural mutations in the hepatitis B virus reverse transcriptase domain associated with hepatocellular carcinoma.
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: 24790911
2014
Annals of laboratory medicine
Abstract: The remaining showed the following mutation patterns: rtM204I/V (50.2%), rtL180M (39.2%), and rtA181T/V (19.6%).
Result: The rtM204I/V mutation (50.2%) was most frequently detected, followed by rtL180M (39.2%) and rtA181V/T (19.6%) mutations.
Discussion: In our study, as expected, the rtM204I/V and rtL180M mutations related to lamivudine resistance were the most frequent, followed b
Amino acid polymorphism in the reverse transcriptase region of hepatitis B virus and the relationship with nucleos(t)ide analogues treatment for preventing mother-to-infant transmission.
HBV mutation literature information.
PMID: 
2014
Drug design, development and therapy
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