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.
Result: All three clones derived from the sample collected in 1999, during the first lamivudine treatment, showed two lamivudine resistant mutations (L526M and
[A study on detection method of lamivudine related mutations in hepatitis B virus polymerase gene].
PMID: 15340520
2004
Zhonghua shi yan he lin chuang bing du xue za zhi
Abstract: Mutation in the tyrosine methionine aspartic aspartic acid (YMDD) motif of HBV polymerase gene was found in eight patients and mutations of YMDD motif associated with L526M were found in another three patients.
[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).
Evolution of hepatitis B virus sequence from a liver transplant recipient with rapid breakthrough despite hepatitis B immune globulin prophylaxis and lamivudine therapy.
1Abstract: These mutations caused L426I/L526M/M550I triple mutation (equivalent to L428I/L528M/M552I in previous reports) in the polymerase, and D144E mutation in the ""a"" determinant of HBsAg."
Abstract: Our study suggests that mutations in the HBsAg (D144E) and the polymerase (L426I/L526M/M550I) of HBV genome may be responsible for viral breakthrough despite HBIG prophylaxis and lamivudine therapy.
Efficacy of famciclovir in the treatment of lamivudine resistance related to an atypical hepatitis B virus mutant.
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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