Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains.
Abstract: Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants.
Mechanism of entecavir resistance of hepatitis B virus with viral breakthrough as determined by long-term clinical assessment and molecular docking simulation.
PMID: 19933798
2010
Antimicrobial agents and chemotherapy
Abstract: Multivariate logistic regression analysis adjusted for age, gender, HBV DNA levels, and LVD resistance (LVDr) (L180M and M204V, but not M204I) indicated that T184 substitutions and S202G (not S202C) were a significant factor for BT (adjusted odds ratio [OR], 141.12, and 95% confidence interval [CI], 6.94 to 2,870.20; OR, 201.25, and 95% CI, 11.22 to 3608.65, respectively).
Prevalence and clinical characterization of patients with acute hepatitis B induced by lamivudine-resistant strains.
PMID: 20074155
2010
Journal of gastroenterology and hepatology
Abstract: LMV-resistance mutations (L180M, M204I) were detected in a patient with subgenotype C2 who had acute self-limited hepatitis.
Hepatitis B viral surface mutations in patients with adefovir resistant chronic hepatitis B with A181T/V polymerase mutations.
PMID: 20119580
2010
Journal of Korean medical science
Introduction: Patients with lamivudine (LMV)-resistant rtM204I/V (+-rtL180M) mutations in the catalytic tyrosine-methionine-aspartate-aspartate (YMDD) motif are less responsive to entecavir (ETV).
Method: These patients developed ADV resistance while undergoing ADV monotherapy as rescue therapy for LMV-resistant HBV (rtM204I/V+-rtL180M).
Discussion: It is possible that these amino acid substitutions were caused by a remaining LMV-resistant mutation, though a rtM204I/V mutation was not detected in sequencing analysis.
Identification and characterization of clevudine-resistant mutants of hepatitis B virus isolated from chronic hepatitis B patients.
Abstract: A quadruple mutant (L129M, V173L, M204I, and H337N) was identified that conferred greater replicative ability and strong resistance to both CLV and lamivudine.
Abstract: In conclusion, the mutation M204I in HBV RT plays a major role in CLV resistance and leads to viral BT during long-term CLV treatment.
Abstract: In vitro phenotypic analysis showed that the mutation M204I was predominantly associated with CLV resistance, whereas L229V was a compensatory mutation for the impaired replication of the M204I mutant.
Abstract: Several conserved mutations were identified in the RT domain during viral BT, with PMID: 20169198
2010
PloS one
Abstract: Changes in the HBV polymerase reverse-transcriptase (RT) domain involve lamivudine-resistance (LVDr) substitutions in the conserved YMDD motif (M204V/I +/- L180M), plus an additional ETV-specific change at residues T184, S202 or M250.
Discussion:
Discussion: An additional unanswered issue is why ETVr substitutions leading to virologic breakthrough occur only in LVDr HBV with the M204V+L180M substitutions and not M204I HBV.
Discussion: However, high level phenotypic resistance does not occur when ETVr substitutions are present with only the M204I LVDr substitution and does not result in virologic breakthrough.
Hepatitis B virus drug resistance in HIV-1-infected patients taking lamivudine-containing antiretroviral therapy.
Abstract: All 19 patients with HBV-DR had lamivudine resistance with the mutations as follows: M204V/I (95%), L180M/A181T (95%), L80V/I (47%), V173L (32%), and N236T (21%).
[Polymerase region mutations and hepatitis B virus genotypes in chronic hepatitis B patients with poor response to lamivudine].
Abstract: M204I mutation in genotype B (20.6%) was more frequent than that in genotype C (13.9%) (x2=4.91, P less than 0.05).
Abstract: The overall incidence rate of A181V/T mutation in genotype C (5.3%) was significantly higher than that in genotype B (0.4%) (x2=12.23, P less than 0.01), but the incidence rate of M204I/V, L180M, T184A/G/I/S, S202G/I and V173L mutations was not significantly different between genotype B and C (each P more than 0.05).
Monitoring of hepatitis B virus surface antigen escape mutations and concomitantly nucleos(t)ide analog resistance mutations in Turkish patients with chronic hepatitis B.
PMID: 20382061
2010
International journal of infectious diseases
Abstract: Interestingly, the treatment-naive patients had preexisting drug resistance mutations related to lamivudine (rtL180M+rtM204I), adefovir (rtA181V, rtQ215S, rtI233V), entecavir (intermediate susceptibility with rtL180M+rtM204IHBV variant), telbivudine (rtL180M+rtM204I), and tenofovir (rtA194T).
Application of hepatitis B virus replication mouse model.
PMID: 20419834
2010
World journal of gastroenterology
Abstract: To identify the model's value in a replication ability study of HBV drug-resistant mutants and a HBx-minus mutant, telbivudine resistance mutants (rtM204I, ayw subtype), adefovir resistance mutants (rtA181V + rtN236T, ayw subtype) and HBx-minus mutants were injected respectively, and their corresponding HBV DNA replication intermediates in mouse liver were assessed.
HBV mutation literature information.
PMID: 
2010
Journal of virology
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