Abstract: Furthermore, the HBsAg-mutation sP217L, silent in RT, significantly correlated with M204V/I-related virological-breakthrough and increased HBsAg-quantification in cell-lysate.
Biochemical and Structural Properties of Entecavir-Resistant Hepatitis B Virus Polymerase with L180M/M204V Mutations.
Abstract: A plasma sample obtained at the first observation was tested for HBV mutants in the polymerase region by direct sequencing; the antiviral drug-resistant rtM204V/I mutations, the most frequent HBV mutants in Italy, were also sought by the more sensitive allele-specific polymerase chain reaction (PCR).
Abstract: AIMS: To detect HBV rtM204V/I lamivudine-resistant strains in serum of patients with acute hepatitis B and to assess their biological and clinical significance.
Abstract: CONCLUSI
Abstract: Compared with those with the HBV wild strain, patients with rtM204V/I more frequently showed severe acute hepatitis B (36.4% vs 8.7%; p < 0.05) and lower values of serum HBV DNA (1.77 x 10(6) +- 4.76 x 10(6) vs.
[Identification of hepatitis B virus YMDD point mutation using peptide nucleic acid clamping PCR].
Abstract: METHODS: RtM204I (ATT) mutant, rtM204V (GTG) mutant and rtM204 (ATG) wild-type plasmids mixed at different ratios were detected for mutations by PNA clamping PCR assay and direct sequencing, and the sensitivity and specificity of the two methods were compared.
Virological Response and Muscular Adverse Events during Long-Term Clevudine Therapy in Chronic Hepatitis B Patients.
Result: One patient had a mixed pattern of rtM204I/V and rtL180M mutations.
Discussion: Resistant mutations were rtM204I and/or rtM204V and/or rtL180M; these are well-known antiviral resistant mutations in HBV DNA against lamivudine and telbivudine.
Dynamics of hepatitis B virus resistance substitutions correlates with virological response in lamivudine-refractory patients with entecavir rescue monotherapy.
Abstract: LMV-resistant mutations (rtL180M and/or rtM204VI) were detected in 9 patients before ETV treatment and not in another 5 patients before and after the treatment.
[Detection of resistance mutations in chronic hepatitis B patients receiving antiviral therapy for over one year].
Abstract: In five of nine samples primary and compensatory multiple mutations (L180M + M204I in one sample, L80I + L180M + M204I in two samples, L80I/V + M204I in one sample) and primary single mutations associated with LVD resistance (M204I/V) in four samples were detected by Inno-Lipa HBV DRv2.
Abstract: Multiple mutations that comprise L180M + M204I in four and L180M + M204V in one sample and single mutations (M204I) in three samples were identified by SEQ.
[HBV vaccine escape mutations in a chronic hepatitis B patient treated with nucleos(t)ide analogues].
Abstract: Primary drug resistance mutations (rtV173L + rtL180M + rtM204V) to lamivudine and telbivudine and a compensatory mutation (rtQ215H) to lamivudine and adefovir were described in the HBV pol gene sequence.
Decreased antigenicity profiles of immune-escaped and drug-resistant hepatitis B surface antigen (HBsAg) double mutants.
Abstract: All five ELISA kits manifested similar avidity, which were demonstrated by the slope of the curves, for the sT118M mutant, and sT118M-rtM204I (sT118M-sI195M) and sT118M-rtM204V (sT118M-sW196S) double mutants, suggesting that drug-resistant YMDD mutants caused negligible losses in the antigenicity of immune-escaped
Profile of hepatitis B virus resistance mutations against nucleoside/nucleotide analogue treatment in Chinese patients with chronic hepatitis B.
Introduction: According to previously studies, the patterns of genotypic resistance in the HBV polymerase can be categorized into five specific evolutionary pathways, including L-nucleoside pathway (rtM204I [or V or I/V]), the acyclic phosphonate pathway (rtN236T), the shared pathway (rtA181T [or V or T/V]) of both L-nucleoside and acyclic phosphonate, ETV resistance pathway (rtL180M+rtM204V with one of either rtT184, S202 or M250 residue changes) and multidrug resistance pathways (rt
Table: M204V
Detection of lamivudine-resistant variants and mutations related to reduced antigenicity of HBsAg in individuals from the cities of Santos and Sao Paulo, Brazil.
Result: Modifications within the POL gene were observed in 9 out of 34 samples (26.47%); we found only one case with the rtM204V mutation, which caused complete resistance to LAM, along with the compensatory mutation rtL180M (2.94%).
Result: When the genes were analyzed together, 9 of the 34 samples had mutations in both genes, and we found the following combinations: sM133L + sI195T with rtL80F + rtT128P, sI195M with rt