literature

HBV mutation literature information.

High-resolution melting and real-time PCR for quantification and detection of drug-resistant HBV mutants in a single amplicon.

PMID: 22301217 2012 Antiviral therapy

Abstract: HRM analysis produced distinct melting temperatures that clearly distinguished the mutants, rtM204V/I (LMV), rtA181V and rtN236T (ADV), and rtT184G and rtM250V (ETV), from their respective wild types.

Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome.

PMID: 22666402 2012 PloS one

Method: NA-resistance-related aa substitutions outside the B and C domains, such as rtI233V, rtN236T and rtM250I/V, were not considered relevant for the aims of the study, since they had not been detected during follow-up in any of the patients studied.

Discussion: In addition, due to the 250-bp-length limitation of the standard GS-FLX chemistry, the relevant NA-resistant substitutions, rtI233V and rtN236T linked to ADV treatment failure, and rtM250I/V linked to ETV failure, located outside the B and C HBV RT functional doma

Prevalence and significance of Hepatitis B reverse transcriptase mutants in different disease stages of untreated patients.

PMID: 22882650 2012 Liver international

Method: The primary drug resistant mutations were defined as nucleotide mutation(s) caused an amino acid substitution that resulted in reduced susceptibility to an antiviral drup, such as rtL180M, rt204I/V for lamivudine, rtL180M+rtM204I/V+rtS202C or rtM250I/V for entecavir; rtA181T/V, rtN236T for adefovir dipivoxil; rtM204I for telbivudine.

Effects of antiviral therapy on the recurrence of hepatocellular carcinoma after curative resection or liver transplantation.

PMID: 23166535 2012 Hepatitis monthly

Introduction: However, in the presence of rtM204I/V mutations, ETV resistance arose with the coexistence of rtI169T, rtL180M, rtT184A/F/G/I/L/S, rtS202G/I, or rtM250V mutations.

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.

PMID: 22224083 2011 Hepatitis monthly

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

Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B.

PMID: 21933446 2011 BMC cancer

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.

Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs.

PMID: 21920388 2011 Antiviral research

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-

Large-scale survey of naturally occurring HBV polymerase mutations associated with anti-HBV drug resistance in untreated patients with chronic hepatitis B.

PMID: 21692935 2011 Journal of viral hepatitis

Abstract: Four patients had the rtI233V mutation that may reduce sensitivity to adefovir, and three patients had the rtM250L/V mutation typical of entecavir resistance.

Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection.

PMID: 21392168 2011 Journal of viral hepatitis

Method: The rtT184A/C/F/G/I/L/M/S, rtS202C/G/I and rtM250I/L/V were defined as the signature ETV-resistant mutations (ETV-R) if concomitant with rtM204I/V.

Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil.

PMID: 21127728 2010 Mediators of inflammation

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

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