Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations.
Conclusion: Under the latter therapeutic scheme, only ephemerally and with minor contribution (~5%), the A181T and T184L lamivudine-adefovir and entecavir resistance-associated mutations were detected, respectively.
Table:
Discussion: In spite of the fact that the A181T adefovir-resistance and the T184L entecavir-resistance mutations were present in the background, they were only minor components of the HBV quasispecies that emerged once tenofovir was added in two consecutive samples separated by a five-month interval.
Discussion: It was expected to find viral replication impairment when rtA181T mutation was detected under adefovir monotherapy, since this variant has a secretory defect and exerts a dominant negative effect on wild-type HBV virion secretion.
Antiviral drug-associated potential vaccine-escape hepatitis B virus mutants in Turkish patients with chronic hepatitis B.
PMID: 21784687
2011
International journal of infectious diseases
Abstract: RESULTS: Seven types of ADAPVEM were detected in the total CHB patients: rtM204V/sI195M, rtM204I/sW196S, rtM204I/sW196L, rtV173L/sE164D, rtA181T/sW172*, rtA181T/
Role of hepatitis B virus genetic barrier in drug-resistance and immune-escape development.
Abstract: rtL80I/V-rtL180M-rtV173L), whilst most primary mutations (including rtM204V-rtA181T/V-rtI169T-rtA194T) are associated with low genetic barrier.
The main hepatitis B virus (HBV) mutants resistant to nucleoside analogs are susceptible in vitro to non-nucleoside inhibitors of HBV replication.
Abstract: HBV reverse-transcriptase (RT) region was sequenced and analyzed for 20 mutations, confirmed by in vitro studies as associated with resistance to nucleos(t)ide HBV-RT inhibitors (rtL80I/V-rtI169T-rtV173L-rtL180M-rtA181T/V/S-rtT184A/S/G/C-rtA194T-rtS202C/G/I-
Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B.
Abstract: A highly sensitive amplification created restriction enzyme site (ACRES) method was devised to detect small amounts of the rtA181T mutant in the serum.
Abstract: BACKGROUND: Development of the hepatitis B virus (HBV) rtA181T/sW172* mutant could occur during prolonged lamivudine (LAM) therapy, conferring cross resistance to adefovir.
Abstract: CONCLUSIONS: Emergence of the rtA181T/sW172* mutant in LAM-resistant patients increased the risk of HCC development in the subsequent courses of antiviral therapy.
Abstract: During the mean follow-up period of 26.2 +- 16.
Virological response to adefovir monotherapy and the risk of adefovir resistance.
PMID: 21941420
2011
World journal of gastroenterology
Abstract: RESULTS: At week 48 and 96, eight (10%) and 14 (18%) of 77 LAM-resistant patients developed the ADV-resistant strain (rtA181V/T and/or rtN236T mutations), respectively.
Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China.
Discussion: reported the incidence rate of rtA181V/T mutation in genotype C was significantly higher than that in genotype B.
Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies.
Discussion: ADV drug resistance detected in this study was found to be associated with mutations at rtN236T and rtA181T/V.
Discussion: However, while the rtN236T substitution does not significantly affect sensitivity to LAM, rtA181T/V and rtQ215S/rtV214A mutations confer partial cross-resistance to LAM.
Discussion: In this study, rtA181T mutations were detected in 6 patients who did not also carry the rt
Lamivudine and adefovir resistance in children and young adults with chronic hepatitis B.
PMID: 19665408
2010
International journal of infectious diseases
Abstract: Three patients developed ADV-associated mutations (A181T), one after 18 months of ADV; the other two had undergone 18 and 36 months of LAM therapy without ADV exposure.
HBV mutation literature information.
PMID: 
2011
BMC infectious diseases
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