Abstract: CONCLUSION: Biochemical response at 12 months from baseline was better in patients with a rtM204I mutation than rtM204V+ rtM204I/V mutations.
Abstract: In addition, early treatment failure was more common in patients with rtM204V+ rtM204I/V mutations than a rtM204I mutation.
Abstract: RESULTS: The baseline tyrosine-methionine-aspartate-aspartate (YMDD) mutation patterns were as follows: rtM204
Differential clinical and virologic impact of hepatitis B virus genotypes B and C on HIV-coinfected patients receiving lamivudine-containing highly active antiretroviral therapy.
Abstract: Clinical and immunologic outcomes in the context of HBV genotypes as well as the emergence of HBV DNA mutations conferring lamivudine resistance (rtM204I/V) were determined.
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
HBV mutation literature information.
PMID: 
2012
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