Abstract: Of the seven patients, six were HBeAg positive at baseline, and four had a double mutation consisting of rtM204V and rtL180M, while two had an rtM204I change.
Prevalence and characterization of lamivudine-resistant hepatitis B virus mutations in HIV-HBV co-infected individuals.
Abstract: Genotypic changes in the YMDD motif (reverse transcriptase [rt] mutations rtM204V/I) conferred resistance to lamivudine as well as reducing the in vitro replication efficiency of HBV.
Abstract: In these patients, rtV173L was invariably found as a third mutation in conjunction with rtL180M and rtM204V.
Selection of a hepatitis B virus strain resistant to adefovir in a liver transplantation patient.
Abstract: RESULTS: Sequence analyses of the HBV polymerase gene revealed a sequential selection of lamivudine resistance mutations L180M+M204V, followed by a reversion to wild-type, and subsequently the selection of a novel adefovir resistance mutation N236T.
Monitoring the emergence of hepatitis B virus polymerase gene variants during lamivudine therapy in human immunodeficiency virus coinfected patients: performance of CLIP sequencing and line probe assay.
Abstract: Interestingly, TRUGENE sequencing identified on late samples from three patients a variant carrying rtV173L plus rtL180M plus M204V mutations, having the in vitro characteristics of 'vaccine escape' mutants.
Mechanism of antiviral activities of 3'-substituted L-nucleosides against 3TC-resistant HBV polymerase: a molecular modelling approach.
Abstract: Analysis of the minimized structure of rtM204V HBV polymerase/3TCTP complex shows that, instead of the steric stress produced by rtV204, a loss of the van der Waals contact around the oxathiolane sugar moiety of 3TCTP caused by the mutation results in the disruption of the active site.
Abstract: As an example, our study shows that the 3'-fluorine atom contributes to the antiviral activity of L-3'-Fd4CTP against rtM204V HBV polymerase by readily compensating for the loss of the van der Waals interaction around the 2',3'-double bond through a formation of a hydrogen bond to the amide backbone of rtD205.
Lamivudine therapy of chronic hepatitis B in three groups of patients: non transplanted patients, liver recipients, and kidney recipients.
PMID: 11938042
2002
Gastroenterologie clinique et biologique
Abstract: After the development of lamivudine resistance, mutations rtM204V and rtL180M were detected in all studied patients, mutation rtM207I in one, with similar results from traditional nucleotide sequencing and a commercial line probe assay.
Mutations in the conserved woodchuck hepatitis virus polymerase FLLA and YMDD regions conferring resistance to lamivudine.
Abstract: Three WHV molecular infectious clones were constructed to study this mutation in greater detail in vitro: A566T, analogous to A181T in HBV; M589V, analogous to the M204V in HBV; and the double mutant A566T/M589V, analogous to A181T/M204V in HBV.
"Restoration of replication phenotype of lamivudine-resistant hepatitis B virus mutants by compensatory changes in the ""fingers"" subdomain of the viral polymerase selected as a consequence of mutations in the overlapping S gene."
Abstract: The LMV-resistant HBV mutants rtM204I and rtL180M/M204V produced substantially weaker HBV DNA replicative intermediate signals by Southern blot analysis and less total intracellular HBV DNA by real-time PCR compared to wild-type virus.
Abstract: The two most common LMV-resistant mutants produce changes in the viral polymerase protein (rt) of rtM204I and rtL180M/M204V (previously rtM550I and rtL526M/
Hepatitis B virus resistance to lamivudine and its clinical implications.
Abstract: These mutations are found at codon (or AA) rtL180M and rtM204V/I in the reverse transcriptase (RT) domain of the HBV polymerase for all genotypes according to a new standardized RT domain numbering system.
HBV mutation literature information.
PMID: 
2003
Journal of viral hepatitis
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