Abstract: Artificial elimination of rtA181C largely restored the rtL180M+A181C+M204V mutant's sensitivity to ETV.
Abstract: CONCLUSIONS: Both clinical and experimental data support rtL180M+A181C+M204V as a novel non-classical ETV-resistance mutation pattern.
Abstract: In clinical practice, undetectable serum HBV DNA was achieved in two of five longitudinally followed rtA181C-positive patients who received switching-to TDF therapy, but not in the other three who received add-on adefovir therapy during observation.
Abstract: Molecular modelling of viral
Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice.
Abstract: Conclusion: An integrated genotypic analysis of HBV RT sequences from patients with chronic HBV treated with ETV led to the discovery of the novel ETVr substitution rtA181C.
Abstract: HBV harboring the rtA181C substitution without LVDr substitutions rtL180M+rtM204V remained susceptible to inhibition by ETV, adefovir, and tenofovir, although cross-resistance to LVD and telbivudine was observed.
Abstract: One LVD-experienced patient-derived HBV RT harboring LVDr substitutions rtL180M+
HBV mutation literature information.
PMID: 
2019
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