Abstract: Additionally, the strategy of switching to ADV monotherapy induced more single rtA181T mutations.
[Clinical characteristics and effect of secondary individualized therapy in chronic hepatitis B patients infected with the rtA181 mutation hepatitis B virus].
Abstract: RESULTS: The rtA181T mutation was found in 64.8% (35/54) of patients with rtA181 mutation HBV.
Abstract: The serological index was determined for carriers of the rtA181T/V mutation.
Abstract: The serum HBsAg level was higher in carriers of the rtA181T mutation than in carriers of the rtA181V mutation (3.80+/-0.45 vs.
[Clinical analysis of hepatitis B virus mutations related to adefovir dipivoxil among patients with chronic hepatitis B virus infection in eastern Zhejiang province].
Abstract: However, long-term use of NAs increases the possibility of developing drug-resistant viral mutations such as the HBV rtA181T/sW172 mutation, which increases the risk of HCC recurrence.
Introduction: Another mutant, rtA181T, may arise during prolonged LAM therapy, conferring cross resistance to ADV.
Introduction: Importantly, since the HBV S and polymerase genes overlap with each other, a great proportion of patients with the rtA181T mutation also carry the SW172 nonsense mutation, resulting in truncation of the preS/S reading frames,
Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation.
Introduction: However, the effect of the rtA181T/sW172* mutation on HBV virology in vivo remains unclear.
Introduction: In this study, a mouse model for the replication of the HBV rtA181T/sW172* mutant was established using a hydrodynamic-based procedure .
Introduction: Previous studies in vitro also demonstrated that the rtA181T/sW172* mutation may impair HBsAg secretion, and may be an oncogenic potential factor leading to advanced hepatocellular carcinoma ( PMID: 23197889
2012
World journal of gastroenterology
Abstract: The rtA181V/T mutations were not suppressed by the LMV-ADV combination therapy.
Abstract: The rtA181V/T mutations were predominantly identified during the ADV treatment in the LMV-resistant patients.
Abstract: Thirty-nine of 64 clones showed an rtA181V/T mutation and six clones showed combined mutations in rt181 and rt236.
Antiviral treatment to prevent chronic hepatitis B or C-related hepatocellular carcinoma.
Abstract: Of the NA resistance-associated mutants, A181T mutant significantly increases the risk of HCC development during the subsequent course of NA therapy.
Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection.
Result: Of the resistance mutations detected in patients who received monotherapies, rtM204I (32.2%), rtM204V + L180M +- V173L (32.2%) and rtM204I + L180M +- V173L (21.0%) were dominant patterns for LAM; rtN236T + A181T and/or rtA181V (34.3%), rtN236T (31.4%) and rtA181V (28.6%) were dominant patterns for ADV, and mutations containin
Detection of lamivudine- or adefovir-resistant hepatitis B virus mutations by a liquid array.
PMID: 21513743
2011
Journal of virological methods
Abstract: A novel polymerase chain reaction (PCR)-Luminex assay was developed for rapid, accurate, and high-throughput detection of the most important hepatitis B virus (HBV) variants, including those with reverse transcriptase (RT) domain L180M, M204I/V, A181T/V/S, I233V and N236T mutations associated with resistance to lamivudine (LAM) or adefovir (ADV).
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: A181T
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 o
HBV mutation literature information.
PMID: 
2012
Antiviral research
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