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 HBV mutation literature information.


  Molecular modeling and biochemical characterization reveal the mechanism of hepatitis B virus polymerase resistance to lamivudine (3TC) and emtricitabine (FTC).
 PMID: 11312349       2001       Journal of virology
Abstract: The effects of Leu528Met, Met552Ile, and Met552Val mutations on the binding of HBV polymerase inhibitors and the natural substrate dCTP were evaluated using an in vitro HBV polymerase assay.
Abstract: The effects of the Leu528Met mutation, which also occurs ne
Abstract: The results from the in vitro studies were as follows: (i) dCTP substrate binding was largely unaffected by the mutations, with Km changing moderately, only in a range of 0.6 to 2.6-fold; (ii) K(i)s for 3TCTP and FTCTP against Met552Ile/Val mutant HBV polymerases were increased 8- to 30-fold; and (iii) the Leu528Met mutation had a modest effect on direct binding of these beta-L-oxathiolane ring-containing nucleotide analogs.


  Detection of hepatitis B virus resistance to antivirals.
 PMID: 11397661       2001       Journal of clinical virology
Abstract: Recent reports on larger series of patients pointed that other mutations residing outside of the C domain but mainly in the B domain of the viral polymerase (L528M) could be associated with these mutations in the YMDD motif.
Abstract: The lamivudine resistant mutants, selected in vivo, can be classified in 2 main groups: group I with a double mutation L528M and M552V, and group II with a single mutation M5521.


  Efficacy and tolerability of long-term therapy using high lamivudine doses for the treatment of chronic hepatitis B.
 PMID: 11480792       2001       Journal of gastroenterology
Abstract: The YMDD mutation was detected in 12 nonresponder patients (9 YVDD, 2 YIDD, and 1 mixed population Y(V/I)DD), generally associated with the L528M mutation.


  Factors associated with hepatitis B virus DNA breakthrough in patients receiving prolonged lamivudine therapy.
 PMID: 11584376       2001       Hepatology (Baltimore, Md.)
Abstract: There was no increase in the rate of development of YMDD variants or L528M mutation in patients receiving lamivudine 25 mg daily or famciclovir 500 mg 3 times a day before being given lamivudine 100 mg daily.


  In vivo dynamics and pathogenicity of wild-type and resistant Hepatitis B virus during long-term lamivudine monotherapy - a clinical note.
 PMID: 10996115       2000       Journal of clinical virology
Abstract: Nineteen weeks later, the virus exhibited additional resistance-associated mutations (L528M and I552V).


  Genotypic succession of mutations of the hepatitis B virus polymerase associated with lamivudine resistance.
 PMID: 11020004       2000       Journal of hepatology
Abstract: Breakthrough viremia was not associated with the single L528M mutation.
Abstract: CONCLUSION: Our observations show that the virus populations conferring resistance to lamivudine can evolve from single to double mutations at amino acid 552 and 528 of the HBV polymerase, and that M552I/ L528M or M552V/L528M seem to be the predominant mutations arising during long-term antiviral therapy with lamivudine.
Abstract: In the majority of lamivudine-resistant isolates the mutations have been reported to occur within the YMDD motif of the viral polymerase, either as a single mutation M552I or as M552V concomitant with  PMID: 11050059       2000       Hepatology (Baltimore, Md.)
Abstract: Determination of viral genotype, precore mutants, and polymerase gene mutants (L528M, M552V, M552I) was performed using the research version of Lipa-HBV.


  Clearance of the original hepatitis B virus YMDD-motif mutants with emergence of distinct lamivudine-resistant mutants during prolonged lamivudine therapy.
 PMID: 10827158       2000       Hepatology (Baltimore, Md.)
Abstract: Of the 23 patients included, 13 harbored either one or a mixture of the two common YMDD-motif mutants (methionine 552-to-isoleucine [M552I] and leucine 528-to-methionine/methionine 552-to-valine [L528M/M552V]) throughout the course, whereas in the remaining 10 patients, distinct mutants became dominant over the original mutants to cause continuing chronic hepatitis.
Abstract: Of them, 3 developed an alanine 529-to-threonine (A529T) mutant, 6 developed a leucine 528-to-methionine/methionine 552-to-isoleucine (L528M


  Evolution of hepatitis B virus polymerase gene sequence during famciclovir therapy for chronic hepatitis B.
 PMID: 10762559       2000       The Journal of infectious diseases
Abstract: No mutation in the YMDD motif was observed, whereas an L528M mutation was clearly selected by famciclovir treatment in 2 patients, as well as 14 novel mutations in 7 patients.


  Line probe assay for monitoring drug resistance in hepatitis B virus-infected patients during antiviral therapy.
 PMID: 10655370       2000       Journal of clinical microbiology
Abstract: A set of 38 highly specific oligonucleotide probes covering three different codon positions, L528M, M552V/I, and V/L/M555I, were selected.



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