HBV mutation literature information.


  Lamivudine plus adefovir or entecavir for patients with chronic hepatitis B resistant to lamivudine and adefovir.
 PMID: 20646776       2010       Journal of hepatology
Abstract: Multivariable analysis showed that LAM+ADV group (OR=0.08, CI=0.02-0.28) and the presence of the rtA181V/T mutation (OR=0.21, CI=0.05-0.91) were independently associated with a decreased rate of virologic response (HBV DNA <2000 IU/ml) at 12 months.


  [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: 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 the patients with combination therapy, the LAM resistance mutation patterns of M204V+L180M, M204V+L180M+L229V, M204I+L80I, and M204V+L180M+V207I were predominant, the ETV resistance mutation T184I/S and S202G


  Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery.
 PMID: 20875460       2010       Antiviral research
Abstract: Among the 10 well-characterized N(t)RTI-resistance mutations, L80I/V, V173L, L180M, A181T, T184S, S202G and M204I/V were significantly associated with treatment with lamivudine, an l-nucleoside analog, and A181S/T/V and N236T were significantly associated with treatment with adefovir, an acyclic nucleoside phosphonate.
Result: Twelve mutations at the eight of these 10 positions were significantly associated with N(t)RTI therapy (Fisher's Exact test; Benjamini-Hochberg adjusted p value <0.01): L80I/V, V173L, L180M,


  A classification model for G-to-A hypermutation in hepatitis B virus ultra-deep pyrosequencing reads.
 PMID: 20937597       2010       Bioinformatics (Oxford, England)
Abstract: For example, two of the most common hepatitis B virus (HBV) reverse transcriptase (RT) drug-resistance mutations, A181T and M204I, arise from G A changes and are routinely detected as low-abundance variants in nearly all HBV deep sequencing samples.
Abstract: The 2.9% of sequence reads that were classified as hypermutated by our model included most of the reads with A181T and/or M204I, indicating the usefulness of this model for distinguishing viral adaptive changes from host-mediated viral editing.


  Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil.
 PMID: 21127728       2010       Mediators of inflammation
Abstract: In contrast, Th1/Th2 cytokines producing T cells remained lower in one patient detected with adefovir dipivoxil resistant HBV A181T/V mutation.
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.
Discussion: Although these mutations were not reported in an earlier study of patients in China, we have detected HBV A181T/I


  Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient.
 PMID: 22312387       2010       Hepatitis monthly
Discussion: But, the rtN236T mutation responsible for primer ADV drug resistance (besides rtA181V/T) found by LIPAwas never detected in direct sequencing.
Discussion: Three primer drug resistance mutations in different domains of HBV viral polymerase, the rtA181V/T, rtL180M+ rtM204V mutations and the rtN236T mutation, were characterized in the same genome, which might explain the multidrug-resistance profile.


  Complex dynamics of hepatitis B virus resistance to adefovir.
 PMID: 19065672       2009       Hepatology (Baltimore, Md.)
Abstract: UNLABELLED: In patients with hepatitis B e antigen-negative chronic hepatitis B, adefovir dipivoxil administration selects variants bearing reverse transcriptase rtN236T and/or rtA181V/T substitutions in 29% of cases after 5 years.


  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
Abstract: UDPS detected drug-resistance mutations that were not detected by PCR in 10 samples from 5 NRTI-treated patients, including the lamivudine-resistance mutation V173L (in 5 samples), the entecavir-resistance mutations T184S (in 2 samples) and S202G (in 1 sample), the adefovir-resistance mutation N236T (in 1 sample), and the lamivudine and adefovir-resistance mutations V173L, L180M, A181T, and M204V (in 1 sample).
Result: Among the NRTI-resistance mutations, M204I was detected in 1.3% of the sequence reads in the sample from subject A7; A181T and M204I were present in 1.0% of the sequence reads in th


  Characterization of hepatitis B virus reverse transcriptase sequences in Chinese treatment naive patients.
 PMID: 19486254       2009       Journal of gastroenterology and hepatology
Abstract: The M204V/I mutation was found in 1.8% of the strains, 1.2% had L180M+ M204V/I, 0.6% had A181T/V, and only one had all three mutations.


  Adefovir dipivoxil resistance patterns in patients with lamivudine-resistant chronic hepatitis B.
 PMID: 19578241       2009       Antiviral therapy
Abstract: ADV resistance mutations (rtA181V/T and rtN236T) were detected alone or in combination for 11/14 patients, whereas novel substitutions were present in 3 patients.
Abstract: Before ADV treatment, apart from 3TC resistance signature mutations, additional changes were found, including the rtA181T mutation, which was already present in 2/14 ADV-resistant patients.
Abstract: CONCLUSIONS: Although most patients showed virological breakthrough because of the well known rtA181V/T and rtN236T substitutions, more complex patterns were also found.



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