The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound.
Abstract: CONCLUSION: The rtA181T/sW172* variant has a secretory defect and exerts a dominant negative effect on wild-type HBV virion secretion.
Abstract: Examination of sequential HBV DNA levels in patients failing lamivudine or adefovir therapy where only the rtA181T change was detected via polymerase chain reaction sequencing revealed that viral load rebound did not occur or was not as large as usually observed with drug-resistant HBV.
Abstract: In vitro analysis revealed that the rtA181T/sW172* variant is not only defective in secretion of viral particles causing intracellular retention of surface
The oncogenic potential of hepatitis B virus rtA181T/ surface truncation mutant.
Abstract: BACKGROUND: Previously, a less prevalent lamivudine-resistant mutant (rtA181T) was discovered in Taiwanese patients, in which a stop codon in the surface gene concomitantly occurred, leading to impaired secretion of hepatitis B virus (HBV) surface antigen.
Abstract: CONCLUSION: Our data indicate that an HBV polymerase rtA181T/surface truncation mutant could emerge spontaneously without previous antiviral treatment.
Abstract: Here, we aimed to evaluate the oncogenic potential of HBV rtA181T/surface truncation mutant.
Abstract: The rt PMID: 19119245
2008
The Korean journal of hepatology
Abstract: At 12 months after ADV treatment, the cumulative rates of HBeAg loss and seroconversion were 15.8% and 10.5%, respectively, and the rtN236T and rtA181T/V mutants in HBV DNA polymerase were identified in 25% and 64% of patients, respectively.
Adefovir for chronic hepatitis B treatment: identification of virological markers linked to therapy response.
Abstract: BACKGROUND: HBV variants rtA181V/T, rtN236T and rtl233V, which confer resistance to adefovir dipivoxil (ADV), are not detected in many non-responding patients.
Primary resistance, multidrug resistance, and cross-resistance pathways in HBV as a consequence of treatment failure.
Abstract: Finally, in highly drug-experienced patients, clusters of mutations such as rtA181T/I233V/N236T/M250L, all on the one dominant HBV genome, are being detected which are associated with multi-drug resistance.
Abstract: Several major HBV-evolutionary NA-resistance pathways (rtM204I/V, rtN236T and rtA181T/V) have now been characterised.
Abstract: The third pathway, rtA181T/V, is associated with resistance to LMV and ADV and is a potential multi-drug resistance pathway and will probably have an impact on
"Molecular analysis of hepatitis B virus ""a"" determinant in asymptomatic and symptomatic Mexican carriers."
Abstract: The rtN236T, rtA181V/T and rtI233V were not identified before ADV therapy and the genotypic mutation of rtN236T was detected in one (3.4%) patient.
In vitro susceptibility of adefovir-associated hepatitis B virus polymerase mutations to other antiviral agents.
Abstract: METHODS: To investigate the in vitro activity of adefovir and other anti-HBV agents against these mutants, we generated five stable cell lines that each expressed one of the following HBV mutants: rtN236T, rtA181V, rtA181V + rtN236T, rtA181T + rtN236T and rtA181T.
Abstract: The rtA181T mutation has also been observed at low frequency, alone or in combination with rt
[A case of chronic hepatitis B with primary adefovir resistance].
Abstract: On the 11th month resistance to adefovir was analysed and rtA181T mutation was found by DNA sequence analysis (Big Dye Terminator Cycle Sequencing kit, Applied Biosystems, USA).
Low resistance to adefovir combined with lamivudine: a 3-year study of 145 lamivudine-resistant hepatitis B patients.
Abstract: The 1-, 2-, 3-, and 4-year cumulative rates of de novo rtA181T were 1%, 2%, 4%, and 4%, respectively.
Abstract: The rtA181V/T was the only adefovir-related mutation detected, which occurred in 6 patients at baseline (4%; 1 rtA181V and 5 rtA181T) and in an additional 3 patients (2%; all rtA181T) during treatment.
HBV mutation literature information.
PMID: 
2008
Hepatology (Baltimore, Md.)
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