Abstract: In addition, ETV resistance mutations (rtL180M+rtT184A+rtS202G+rtM204V) were detected in one patient.
Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection.
Abstract: In rtS202G mutants (plus lamivudine resistance), addition of either PC or BCP mutations moderately enhanced the reduced replication, without reaching WT HBV levels.
Abstract: Our data demonstrate that HBeAg-suppressing PC or BCP mutations cannot restore the strongly reduced replicative capacity of ETV-resistant HBV mutants to WT level, although they moderately increase replication of rtS202G combination mutants.
Abstract: To comprehensively analyse the impact of PC or BCP mutations on viral replication of ETV-resistant HBV mutants, replication-competent HBV constructs wer
Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil.
Method: In brief, serum HBV DNA was amplified by PCR and pyrosequenced to detect the following mutations of HBV polymerase: I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T, S202G/I, M204V/I, N236T, and M250V.
Result: The serum samples of these two patients were examined for ten HBV mutations (I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T
Mechanism of entecavir resistance of hepatitis B virus with viral breakthrough as determined by long-term clinical assessment and molecular docking simulation.
PMID: 19933798
2010
Antimicrobial agents and chemotherapy
Abstract: Modeling of HBV reverse transcriptase (RT) by docking simulation indicated that a combination of LVDr and ETVr (T184L or S202G) was characterized by a change in the direction of the D205 residue and steric conflict in the binding pocket of ETV triphosphate (ETV-TP), by significantly longer minimal distances (2.2 A and 2.1 A), and by higher potential energy (-117 and -99.8 Kcal/mol) for ETV-TP compared with the wild type (1.3 A; -178 Kcal/mol) and LVDr substitutions (1.5 A; -141 Kcal/mol).
Abstract: Multivariate logistic regression analysis adjusted for age, gender, HBV DNA levels, and LVD resistance (LVDr) (L180M and M204V, but not M204I) indicated that T184 substitutions and S202G (not
Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir.
Result: Additionally, large substitutions S202F/I/Y and small substitutions S202G/A were highly resistant.
Result: Figure 2B shows that introduction of the S202G substitution causes repositioning of the L180M and M204V residues to further restrict the ETV-TP binding site.
Result: Several different ETVr substitutions have been observed in ETV-treated patients, including T184A/C/F/G/I/L/M/S, S202C/G/I, and M250 I/L/V.
Result: The results of comprehensive phenotypic analysis of substitutions at positions S202 indicated that S202A/G/C/T/V/N replicated well a
[Polymerase region mutations and hepatitis B virus genotypes in chronic hepatitis B patients with poor response to lamivudine].
Abstract: The overall incidence rate of A181V/T mutation in genotype C (5.3%) was significantly higher than that in genotype B (0.4%) (x2=12.23, P less than 0.01), but the incidence rate of M204I/V, L180M, T184A/G/I/S, S202G/I and V173L mutations was not significantly different between genotype B and C (each P more than 0.05).
Acute hepatitis B infection associated with drug-resistant hepatitis B virus.
Abstract: RESULTS: Direct PCR sequencing showed that 14 samples (7.0%) were positive for drug-resistant HBV variants, comprised of 11 with the lamivudine-resistant pattern rtM204I and/or rtM204V in the presence and absence of compensatory mutations rtL80I, rtV173L, and rtL180M; two with the adefovir-resistant pattern rtA181V; and one with the entecavir-resistant pattern rtL180M+rtS202G+rt
[Detection of HBV resistant mutations related to lamivudine, adefovir and entecavir by reverse hybridization technique].
Abstract: To detect non-synonymous amino acid substitutions associated with lamivudine, adefovir and entecavir, 26 specific oligonucleotide probes covering ten different codon positions, I169T, V173L/G, L180M, A181T/V, T184G, S202I/G, M204V/I, Q215S, N236T and M250V/I/L were synthesized and immobilized on nylon membranes charged positively.
[Evolution of hepatitis B virus quasispecies during lamivudine-entecavir sequential therapy].
Abstract: The rtL180M+S202G+M204V triple mutant, which was most likely a descendant of the LAM resistant rtL180M+M204V variant, was closely correlated with ETV resistant in Patient II.
HBV mutation literature information.
PMID: 
2011
Annals of hepatology
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