Discrepancy of potential antiviral resistance mutation profiles within the HBV reverse transcriptase between nucleos(t)ide analogue-untreated and -treated patients with chronic hepatitis B in a hospital in China.
Abstract: Substitutions at seven non-classical mutation sites were of interest due to either detection only in patients with virologic breakthrough (rtL82 and rtV214), or potential ties with HBV genotypes (rtV191 and rtL229), or coexistence with rtM204I/V (rtL229), or increased mutation trends after NA-treatment (rtT128, rtV207, and rtN/H238).
Pre-existing YMDD mutants in treatment-naive patients with chronic hepatitis B are not selected during lamivudine therapy.
Abstract: HRM analysis produced distinct melting temperatures that clearly distinguished the mutants, rtM204V/I (LMV), rtA181V and rtN236T (ADV), and rtT184G and rtM250V (ETV), from their respective wild types.
Decreased infectivity of nucleoside analogs-resistant hepatitis B virus mutants.
Abstract: RESULTS: Forty out of the 120 patients were found to have one or two point mutations associated with drug resistance, including 17 with L180M and M204V/I mutations (42.5%), 10 with M204V/I mutation (25%), 8 with N236T mutation (20%), 3 with L180M mutation (7.5%), and 1 with both A181V/T and N236T mutations (2.5%), and 1 with A181V/T mutation(2.5%).
The rtL229 substitutions in the reverse transcriptase region of hepatitis B virus (HBV) polymerase are potentially associated with lamivudine resistance as a compensatory mutation.
Abstract: CONCLUSION: The rtL229 substitutions were potentially associated with LAM resistance in Chinese patients and rtL229F had characteristics of a compensatory mutation of rtM204I mutant.
Abstract: Functionally, rtL229F did not confer reduced susceptibility to LAM, but could restore replication capacity of rtM204I strain.
Abstract: Replication-competent viral amplicons which harbored HBV genomes of wild-type, rtM204I, or rtM204I in conjunction with various rtL229 substitutions (
Long-term monitoring drug resistance by ultra-deep pyrosequencing in a chronic hepatitis B virus (HBV)-infected patient exposed to several unsuccessful therapy schemes.
Abstract: Under sequential HBV monotherapies including lamivudine, adefovir and entecavir, a high frequency of rtM204I mutation was detected initially as unique and then coexisting with rtM204V.
Convergence and coevolution of hepatitis B virus drug resistance.
Abstract: An analysis of Bayesian networks that connect rtM204I/V to many sites of HBV proteins confirms that lamivudine resistance is a complex trait encoded by the entire HBV genome rather than by a single mutation.
Abstract: Here we show that the rtM204I/V substitution, although essential, is insufficient for establishing resistance against lamivudine.
Abstract: The analysis of 639 HBV whole-genome sequences obtained from 11 patients shows that rtM204I/V is independently acquired by more than one intra-host HBV variant, indicating the convergent nature of lamivudine resistance.
Abstract: Treatment with lamivudine of patients infected with hepatitis B virus (HBV) results in a high rate of drug resistance, which is primarily associated with the
Antiviral therapy against chronic hepatitis B in Brazil: high rates of lamivudine resistance mutations and correlation with HBV genotypes.
PMID: 22510826
2012
Memorias do Instituto Oswaldo Cruz
Abstract: Six out of nine isolates that contained the rtM204I mutation belonged to genotype D and half of them displayed a single mutation.
Dynamics of hepatitis B virus quasispecies in association with nucleos(t)ide analogue treatment determined by ultra-deep sequencing.
Abstract: Moreover, various abundances of clones resistant to NA were common in both the liver and serum of treatment-naïve patients, and the proportion of M204VI mutants resistant to lamivudine and entecavir expanded in response to entecavir treatment in the serum of 35.7% (5/14) of patients, suggesting the putative risk of developing drug resistance to NA.
HBV mutation literature information.
PMID: 
2012
Journal of medical virology
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