Abstract: To detect non-synonymous amino acid substitutions associated with lamivudine, adefovir and entecavir, 26 specific oligonucleotide probes covering ten different codon positions, I169T, V173L/G, L180M, A181T/V, T184G, S202I/G, M204V/I, Q215S, N236T and M250V/I/L were synthesized and immobilized on nylon membranes charged positively.
Lamivudine-resistance mutations can be selected even at very low levels of hepatitis B viraemia.
Abstract: Drug-resistance mutations were observed in 17 (77.2%) LAM-treated patients with virological breakthrough: 8 M204V, 7 M204I, 1 M204I/V, and 1 A181T.
Abstract: Drug-resistance mutations were present also in patients with undetectable serum HBV-DNA: M204I was detected in 2 patients receiving LAM-monotherapy, and V84M in 1 patient receiving LAM+ADV.
[Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance].
Abstract: 20% of clones from three serum samples were detected double resistance to LAM and entecavir (ETV) in the combination therapy group, the resistance patterns were M204I+L80I+T184I (2/10), M204V+L180M+T184S (2/10), and M204V+L180M+G173L+S202G (2/10) respectively.
Abstract: CONCLUSIONS: In the patients with suboptimal viral response to ADV therapy after LAM resistance, the ADV resistance mutation patterns of A181T+N236T, A181V and A181T could easily be selected during ADV monotherapy; while in th
Antiviral activity of various 1-(2'-deoxy-beta-D-lyxofuranosyl), 1-(2'-fluoro-beta-D-xylofuranosyl), 1-(3'-fluoro-beta-D-arabinofuranosyl), and 2'-fluoro-2',3'-didehydro-2',3'-dideoxyribose pyrimidine nucleoside analogues against duck hepatitis B virus (DHBV) and human hepatitis B virus (HBV) replication.
PMID: 20857959
2010
Journal of medicinal chemistry
Abstract: Intriguingly, 25, 39, 48, and 49 retained sensitivity against lamivudine-resistant HBV containing a single mutation (M204I) and 48 emerged as an effective inhibitor of drug-resistant HBV with an EC(50) of 4.1 muM.
Mutation pattern of lamivudine resistance in relation to hepatitis B genotypes: hepatitis B genotypes differ in their lamivudine resistance associated mutation pattern.
Abstract: Future studies will need to evaluate whether this will translate into genotype-specific differences in resistance emergence on either entecavir or telbivudine as these antivirals differ in their mutation profile, rtM204V for entecavir and rtM204I for telbivudine.
Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery.
Abstract: Among the 10 well-characterized N(t)RTI-resistance mutations, L80I/V, V173L, L180M, A181T, T184S, S202G and M204I/V were significantly associated with treatment with lamivudine, an l-nucleoside analog, and A181S/T/V and N236T were significantly associated with treatment with adefovir, an acyclic nucleoside phosphonate.
Result: Twelve mutations at the eight of these 10 positions were significantly associated with N(t)RTI therapy (Fisher's Exact test; Benjamini-Hochberg adjusted p value <0.01): L80I/V, V173L, L180M,
Hepatitis B virus (HBV) subgenotypes C2 and B2 differ in lamivudine- and adefovir-resistance-associated mutational patterns in HBV-infected Chinese patients.
PMID: 20881176
2010
Journal of clinical microbiology
Abstract: The incidence of lamivudine-resistant mutations was significantly higher in HBV/C2 compared to HBV/B2 (27.9% versus 19.8%; P<0.01), and the significant difference was observed only for rtM204I and not rtM204V.
A classification model for G-to-A hypermutation in hepatitis B virus ultra-deep pyrosequencing reads.
Abstract: For example, two of the most common hepatitis B virus (HBV) reverse transcriptase (RT) drug-resistance mutations, A181T and M204I, arise from G A changes and are routinely detected as low-abundance variants in nearly all HBV deep sequencing samples.
Abstract: The 2.9% of sequence reads that were classified as hypermutated by our model included most of the reads with A181T and/or M204I, indicating the usefulness of this model for distinguishing viral adaptive changes from host-mediated viral editing.
Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil.
Discussion: A recent study based in Hong Kong has indeed suggested that M204V/I mutation is associated with the resistance of HBeAg-positive chronic HBV patients to lamivudine and adefovir dipivoxil combination treatment.
Discussion: In the investigation of HBV mutations in adefovir dipivoxil resistance, we have identified HBV A181T/V mutations in one and M204V/I mutations in another of two patients that showed HBV DNA persistence through 104 weeks of adefovir dipivoxil treatment.
Discussion: The HBV L180M and M204V/I mutations are associated with lamivudine resistance and the concept that these mutations can be responsible for adefovir dipivoxil resistance is intriguing and remains to be confirmed i
Profile of HBV antiviral resistance mutations with distinct evolutionary pathways against nucleoside/nucleotide analogue treatment among Chinese chronic hepatitis B patients.
Abstract: rtM204 mutations (27 rtM204I, 15 rtM204V and 5 rtM204I/V cases) were detected at the highest frequency among 65 mutants (72.30% [47/65]) and found to display 16 combination mutation patterns, in which rtM204I and rtM204V were significantly associated with rtL80I/V and rtL180M, respectively (P<0.01).
HBV mutation literature information.
PMID: 
2010
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