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: 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.

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-

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

PMID: 20169198 2010 PloS one

Result: Among those that grew well, both large (T184L/M/F/Q/N) and small (T184A/G/C) residues resulted in ETVr.

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.

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

Result: The serum samples of these two patients were examined for ten HBV mutations (I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T, S202G/I, M204V/I, N236T, M250V) that have been reported in the reverse transcriptase regions of HBV polymerase gene in association with the HBV resistance to the treatment of nucleoside and nucleotide analogs.