Frequency and mutation patterns of resistance in patients with chronic hepatitis B infection treated with nucleos(t)ide analogs in add-on and switch strategies.
Introduction: Two patterns of ETV resistance have been characterized, and they include the LAM-resistance mutation rtM204I/V plus an additional mutation of either rtT184G + rtS202I/C or rtM250V + rtI169T .
Discussion: High levels of ETV resistance resulted from dual rtM250V and rtI169T mutations, and we detected another profile, the rtM204I/V + rt
Role of hepatitis B virus genetic barrier in drug-resistance and immune-escape development.
Abstract: rtL80I/V-rtL180M-rtV173L), whilst most primary mutations (including rtM204V-rtA181T/V-rtI169T-rtA194T) are associated with low genetic barrier.
Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs.
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.
Introduction: However, in the presence of rtM204I/V mutations, ETV resistance can occur if the rtI169T, rtT184A/F/G/I/L/S, rtS202G/I, or rtM250V mutation coexists.
Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil.
Method: In brief, serum HBV DNA was amplified by PCR and pyrosequenced to detect the following mutations of HBV polymerase: I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T, S202G/I, M204V/I, N236T, and M250V.
Result: The serum samples of these two patients were examined for ten HBV mutations (I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T
Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery.
Method: We analyzed the following mutations at 10 well-characterized DRM positions L80IV, I169T, V173L, L180M, A181TV, T184SAILFG, S202GI, M204VIS, N236T, and M250V.
Result: Too few sequences from entecavir-treated individuals were available to identify treatment associations for two (I169T and M250V) of the four (I169T, T184SAILFG, S202GI, M250V) entecavir-associated mutation positions.
[Detection of HBV resistant mutations related to lamivudine, adefovir and entecavir by reverse hybridization technique].
Abstract: RESULTS: The specific probes of 10 codon positions related to HBV wild-type and resistant reference strains, including I169T, V173L, L180M, A181T, T184G, S202I, M204V, Q215S, N236T, M250V, were distinguished effectively by reverse hybridization method.
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, PMID: 20169198
2010
PloS one
Discussion: I169T substitutions were found in both patients initially identified with ETVr and various I169 substitutions have been seen in twelve of our other ETVr patients.
Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients.
PMID: 19301976
2009
The Journal of infectious diseases
Method: Established NRTI-resistance mutations included the following RT mutations: rtL80V/I, rtI169T, rtV173L, rtL180M, rtA181TV, rtT184S/A/I/L/F/G, rtA194T, rtS202G/I, rtM204V/I/S, rtN236T, and rt PMID: 18070286
2007
Journal of viral hepatitis
Abstract: The aim of this study was to determine the prevalence of HBV variants associated with ETV resistance (rtI169T, rtT184G, rtS202I, rtM250V) in naive patients before and during lamivudine therapy.
HBV mutation literature information.
PMID: 
2011
Hepatitis monthly
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