Result: RT sequence changes implicated in adefovir-resistance were detected, including S213T 5.83% (19/325), S213N 0.9% (3/325), V214E 0.61% (2/325), V214A 0.61% (2/325), Q215P 2.75% (9/325), Q215S 7.06% (23/325), Q215H1.53% (5/325), and F221Y 2.76% (9/325) of isolations that previously reported adefovir-resistance mutation (Figure 1).
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.
Result: Single compensatory mutations were not detected in the switch therapy group; however, rtQ215H/P/S +- rtV214A/P mutations were found in 12 out of 88 patients (14%) in the add-on therapy group, and this difference was significant (P < 0.01).
Discussion: Accordingly, in our previously published report, we found that rtQ215A/H/P/S substitutions could be detected as naturally occurring mutations in treatment-naive patients with Discussion: Furthermore, rtQ215H/P/S substitutions occur as dominant compensatory mutations in treatment-naive hemodialysis patients infected with HBV genotype D (unpublished data).
Prevalence, viral replication efficiency and antiviral drug susceptibility of rtQ215 polymerase mutations within the hepatitis B virus genome.
Abstract: In phenotypic assays, rtQ215S, rtQ215P and rtQ215H constructs showed equivalent levels of viral replication as wild-type HBV, whereas LAM- and ADV-resistant mutants had significantly impaired replicative capacities.
Abstract: Replication-competent HBV constructs containing the naturally occurring rtQ215H, rtQ215P and rtQ215S mutations were generated, and compared to wild-type, LAM- (rtM204I, rtL180M/
HBV mutation literature information.
PMID: 
2013
Virology journal
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