literature

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

3Introduction: The region analyzed extends from codon rt148 to rt208 in the P ORF, which includes most RT codons corresponding to reported relevant NA-resistant aa substitutions (rtI169T, rtV173L, rtL180M, rtA181T/V, rtT184S/A/I/L/G/C/M, rtA194T, rtA202C/G/I, rt

PMID: 22224083 2011 Hepatitis monthly

Result: The ETV-resistance mutation rtM204I/V + rtL180M + rtT184A/I/

Discussion: High levels of ETV resistance resulted from dual rtM250V and rtI169T mutations, and we detected another profile, the rtM204I/V + rtL180M + rtT184A/I/S or rtS202C triple mutation, as an ETV-resistant mutation in both NUC therapy strategies.

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.

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.

Table: T184I/L

Table: T184I

[Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance].

PMID: 20678438 2010 Zhonghua gan zang bing za zhi

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

[Polymerase region mutations and hepatitis B virus genotypes in chronic hepatitis B patients with poor response to lamivudine].

PMID: 20380793 2010 Zhonghua gan zang bing za zhi

Abstract: The overall incidence rate of A181V/T mutation in genotype C (5.3%) was significantly higher than that in genotype B (0.4%) (x2=12.23, P less than 0.01), but the incidence rate of M204I/V, L180M, T184A/G/I/S, S202G/I and V173L mutations was not significantly different between genotype B and C (each P more than 0.05).

Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir.

PMID: 20169198 2010 PloS one

Result: T184 I, M, F, substitutions also fit this pattern.

Result: Several different ETVr substitutions have been observed in ETV-treated patients, including T184A/C/F/G/I/L/M/S, S202C/G/I, and M250 I/L/V.

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: 19918102 2009 Antiviral therapy

Abstract: ETV resistance mutations (rtL180M+rtT184I/L[rtS202G]+rtM204V) were detected in five patients with pre-existing rt204 mutations.