HBV mutation literature information.


  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
Result: The 10 most variable RT substitutions observed during sequential NA treatment, blindly selected after SD sorting and all associated with NA resistance (rtL180M, rtM204V, rtS202G, rtV207I, rtA181T, rtL173V, rtI169T, rtV191I, rtM204I, and rtT184A) (Table 3)


  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
Result: The ETV-resistance mutation rtM204I/V + rtL180M + rtT184A/I/S or rtS202C was found in 10 out of 194 patients (5%).
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  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-


  Evolution of hepatitis B virus during long-term therapy in patients with chronic hepatitis B.
 PMID: 21911882       2011       Annals of hepatology
Abstract: In addition, ETV resistance mutations (rtL180M+rtT184A+rtS202G+rtM204V) were detected in one patient.


  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: T184A
Table: T184L/A


  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.


  [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 A and S changes also fit this model.
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.



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