Abstract: An exception is rtM204I, which can derive from a transition or a transversion.
The YMDD and rtA194T mutations result in decreased replication capacity in wild-type HBV as well as in HBV with precore and basal core promoter mutations.
Abstract: rtA194T reduced replication by <40%, whereas rtL180M+rtM204V, Abstract: METHODS: A plasmid containing a wild-type 1.3 genome length genotype D HBV laboratory strain was used as a parent for PC, BCP, rtA194T+-rtL180M+rtM204V, rtL180M+rtM204V and rtM204I mutants.
The main hepatitis B virus (HBV) mutants resistant to nucleoside analogs are susceptible in vitro to non-nucleoside inhibitors of HBV replication.
Abstract: HBV breakthrough occurred in one recipient at the month 12 post-OLT, with detectable serum HBV-DNA (740 copies/mL) and tyrosine-methionine-aspartate-aspartate motif mutation (rtM204I and rtM204V).
Evolution of hepatitis B virus during long-term therapy in patients with chronic hepatitis B.
Abstract: During ADV and LAM treatment, one patient developed ADV plus LAM resistance mutations (rtI163V+rtL180M+rtA181V+rtN236T), in this case, HBV strains harbouring polymerase mutations did not develop LAM associated rtM204V/I primary mutation.
Abstract: RESULTS: Three patients developed LAM resistance mutations (2 presented rtM204I and one rtL180M+rtM204V/I) and one patient showed
Lamivudine resistance mutations in European patients with hepatitis B and patients co-infected with HIV and hepatitis B.
Abstract: HBV reverse-transcriptase (RT) region was sequenced and analyzed for 20 mutations, confirmed by in vitro studies as associated with resistance to nucleos(t)ide HBV-RT inhibitors (rtL80I/V-rtI169T-rtV173L-rtL180M-rtA181T/V/S-rtT184A/S/G/C-rtA194T-rtS202C/G/I-
Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B.
Abstract: Virological factors including HBV-DNA level, genotype, precore G1896A, BCP A1762T/G1764A, rtM204I/V, rtA181T and pre-S internal deletion mutations as well as clinical variables including subsequent use of rescue drugs were submitted for outcome analysis.
Method: The methods to detect HBV basal core promoter (BCP) A1762T/G1764A mutations, precore stop codon
Table: M204I
Molecular epidemical characteristics of Lamivudine resistance mutations of HBV in southern China.
Discussion: Other mutations and mixed combinations were also observed (rtM204I+rtV207M/L, rtM204I+rtV173L, rtM204I+rtS213T, rtM204V+rtL180M+rtV173L/M, rtM204V+rtL180M+rt PMID: 22007495
2011
Sichuan da xue xue bao. Yi xue ban
Abstract: The type of genotype mutation were all rtM204I.