Discussion: HBV variants with combinations of HBs Ag (G145R or P120T) and polymerase (L526M plus M550V) mutations showed increased HBV replication resulting in a severe clinical course in transplanted patients.
Inhibition of hepatitis B virus gene expression and replication by helioxanthin and its derivative.
Abstract: The lamivudine-resistant HBV, L526M/M550V double mutant strain, was also sensitive to helioxanthin and 5-4-2.
Reverse transcriptase activity of hepatitis B virus (HBV) DNA polymerase within core capsid: interaction with deoxynucleoside triphosphates and anti-HBV L-deoxynucleoside analog triphosphates.
Abstract: The L526M and M550V mutations caused a greater decrease in the Vmax using the wt RNA template compared with the G1896A-mutated template.
Abstract: The L526M, M550V, and L526M/M550V mutations caused varying degrees of resistance to the different M-nucleoside triphosphates.
Abstract: The additional L526M mutation increased the efficiency of the M550V-mutated DP but no more than that of the L526M-mutated DP.
Abstract: The use of L(-)SddC [beta-L-2',3'-dideoxy-3'-thiacytidine (lamivudine, 3TC)] for the treatment of Herpes B virus (HBV) infection is hindered by the emerge
Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine.
Abstract: After reinstitution of lamivudine (2002), the predominant HBV population exhibited a rare triple mutation (V519L, L526M, M550V), which has previously been associated with an in vitro reduction of virus antigenicity (escape mutant).
Abstract: RESULTS: HBV isolate derived from a sample collected in 1999 during an antiretroviral treatment with lamivudine showed the lamivudine resistant double mutation (L526M, M550V).
Abstract: The M550V variation may be accompanied by L526M mutation, notably in HIV-HBV co-infected patients.
Abstract: The resistance occurs through M550V or M550I aminoacid replacements.
Introduction: Most of these mutations usual
Increased DNA polymerase fidelity of the Lamivudine resistant variants of human hepatitis B virus DNA polymerase.
PMID: 15469692
2004
Journal of biochemistry and molecular biology
Abstract: From the f(ins) value analysis, it is evident that M550I and M550V exhibit higher fidelity values than the wild-type HBV DNA polymerase, while M550A exhibits similar fidelity values.
Abstract: It is therefore suggested that lamivudine resistance comes from the stringency to dNTP binding and the discrimination of dCTP and lamivudine in M550V and M550I.
Abstract: The FLAG-tagged wild-type (FPolE) and Met550 variants (FPolE/M550A, M550V, and M550I) of HBV DNA polymerases were expressed in insect cells, then purified.
[Quasispecies and mutation of hepatitis B virus polymerase gene in lamivudine- treated patients].
Abstract: By sequencing the predominant clones, there were 2 patients with M550V/L528M mutation, 3 patients with M550I mutation and 1 patient with wild type after lamivudine therapy.
[Analysis of three lamivudine-resistant HBV mutants with the method of restriction enzyme digestion and its application].
PMID: 12870011
2003
Zhonghua shi yan he lin chuang bing du xue za zhi
Abstract: Six of them were infected with M5501 mutant; five were infected with M550V mutant (one of them had both M550V and L526M mutations).
Efficacy of famciclovir in the treatment of lamivudine resistance related to an atypical hepatitis B virus mutant.
Abstract: The severe hepatitic flare consequent to the lamivudine resistance in this patient was successfully treated with famciclovir, indicating that both M550V and M550I mutants with preserved wild-type sequence at position 526 of HBV reverse transcriptase are susceptible to famciclovir.
Abstract: Treatment with famciclovir has not been effective in the majority of patients who developed lamivudine resistance due to methionine-to-valine mutation at position 550, because this mutation has been uniformly associated with leucine-to-methionine mutation at position 526, a mutation that is associated with resistance to famciclovir.
Reduced antigenicity of the hepatitis B virus HBsAg protein arising as a consequence of sequence changes in the overlapping polymerase gene that are selected by lamivudine therapy.
Abstract: HBsAg mutants including E164D, W196S, I195M, M198I, and E164D/I195M (corresponding to the polymerase protein changes of V519L, M550I, L526M/M550V V553I, and V519L/L526M/M550V) selected during lamivudine treatment also demonstrated reduced binding to anti-HBs antibody.
"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 two most common LMV-resistant mutants produce changes in the viral polymerase protein (rt) of rtM204I and rtL180M/M204V (previously rtM550I and rtL526M/M550V).
HBV mutation literature information.
PMID: 
2021
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