Lamivudine resistance and other mutations in the polymerase and surface antigen genes of hepatitis B virus associated with a fatal hepatic failure case.
PMID: 18171343
2008
Journal of gastroenterology and hepatology
Abstract: After 32 months, the rtM204V mutation was predominant, accompanied by the lamivudine-resistant rtL180M mutation.
Abstract: BACKGROUND AND AIM: Resistance to lamivudine therapy of chronic hepatitis B virus (HBV) infection occurs by mutation in the YMDD motif of the reverse transcriptase (rt) domain (rtM204V/I) of the virus polymerase, and is usually accompanied by rtL180M mutation.
Hepatitis B virus genotypes and resistance mutations in patients under long term lamivudine therapy: characterization of genotype G in Brazil.
Abstract: All three showed the double mutation L180M/M204V and displayed a large genetic divergence when compared with other full-length genotype G isolates.
Abstract: Fifteen patients showed the L180M/M204V lamivudine resistant double mutation.
Result: Fifteen patients showed the well-known double rtL180M/rtM204V mutation.
Result: The last one resulted from the lamivudine resistance mutation at rtL180M position.
Discussion: The occurrence of mutations rtL180M and rtV173L ha
Comprehensive evaluation of hepatitis B virus reverse transcriptase substitutions associated with entecavir resistance.
Abstract: Two of these substitutions are associated with lamivudine resistance (LVDr) in the tyrosine-methionine-aspartate-aspartate (YMDD) motif (rtM204V and rtL180M), whereas the other occurs at one or more positions specifically associated with ETV resistance (ETVr): rtT184, rtS202, or rtM250.
[Mutations of HBV polymerase gene sequence in lamivudine-resistant chronic hepatitis B patients].
Abstract: RESULTS: Lamivudine resistant mutation was detected in 103 patients, and the major mutations included rtL180M+rtM204V and rtM204I, accounting for 58.3% and 22.3%, respectively.
Rolling circle amplification, a powerful tool for genetic and functional studies of complete hepatitis B virus genomes from low-level infections and for directly probing covalently closed circular DNA.
PMID: 18606836
2008
Antimicrobial agents and chemotherapy
1Abstract: Only the genomes from the last biopsy specimen obtained after the emergence of lamivudine resistance contained the lamivudine resistance-associated mutations rtL180M and rtM204V (""rt"" indicates reverse transcriptase domain)."
Selection of an entecavir-resistant mutant despite prolonged hepatitis B virus DNA suppression, in a chronic hepatitis B patient with preexistent lamivudine resistance: successful rescue therapy with tenofovir.
PMID: 18617782
2008
European journal of gastroenterology & hepatology
Abstract: Sequence analysis revealed the presence of rtL180M and rtM204V lamivudine-resistant-associated mutations at the start of entecavir treatment.
[A five-year analysis of HBV mutations in a multidrug-resistant patient with chronic hepatitis B].
Abstract: RESULTS: Several mutations were identified in succession, including LAM-resistant mutations M204I/V and L180M+M204V, ETV-resistant mutation S202G, and HBeAg nonsense mutation G1896A.
Supportive role played by precore and preS2 genomic changes in the establishment of lamivudine-resistant hepatitis B virus.
PMID: 18713056
2008
The Journal of infectious diseases
Abstract: BACKGROUND: Hepatitis B virus (HBV) establishes lamivudine resistance via the resistance-causative rtM204V/I mutation and the replication-compensatory rtL180M mutation.
Abstract: CONCLUSIONS: Both the precore-defective mutation and the preS2 deletion may play a supportive role in the replication of lamivudine-resistant HBV, which may be a reason for there being no need for the compensatory rtL180M mutation in lamivudine-resistant HBV possessing the precore and preS2 genomic changes.
Abstract: However, both lamivudine-resistant viruses with and those without rt
Understanding the molecular basis of HBV drug resistance by molecular modeling.
Abstract: In this regard, homology modeled structure of HBV-polymerase was used for minimization, conformational search and induced fit docking followed by binding energy calculation on wild-type as well as on mutant HBV-polymerases (L180M, M204V, M204I, L180M+M204V, L180M-M204I).
Introduction: The aim of present molecular modeling study is to elucidate the structural features of HBV-polymerase in terms of qualitative and quantitative changes conferred by B and C domain mutations (3TC; Lamivudine associated resistance: rtL180M and rt
[YMDD motif variants detected by Inno-Lipa HBV DR assay in chronic hepatitis B patients during lamivudine therapy].
HBV mutation literature information.
PMID: 
2008
Journal of gastroenterology and hepatology
Browser Board
Co-occurred Entities
Filtrator
ViMRT