literature

HBV mutation literature information.

rtM204Q may serve as a novel lamivudine-resistance-associated mutation of hepatitis B virus.

PMID: 24586482 2014 PloS one

Discussion: The rtA181T has been related with LAM exposure and it induces a stop codon (sW172stop) in the overlapping hepatitis B surface protein.

The impact of the hepatitis B virus polymerase rtA181T mutation on replication and drug resistance is potentially affected by overlapping changes in surface gene.

PMID: 24696492 2014 Journal of virology

Abstract: Compared to the rtA181T surface missense mutation (rtA181T/sW172S), the introduction of rtA181T surface nonsense mutation (rtA181T/sW172*) resulted in decreased viral replication and increased drug resistance.

Abstract: Complementation assay revealed that the truncated PreS1 is responsible for reduced replication of rtA181T/s

Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers.

PMID: 25320728 2014 Clinical and molecular hepatology

Discussion: In this regard, we previously found several point mutations in the MHR region and W172stop corresponding to the multidrug-resistant rtA181T mutation in polymerase impair the secretion of both virions and HBsAg.

Hepatitis B virus genotype C encoding resistance mutations that emerge during adefovir dipivoxil therapy: in vitro replication phenotype.

PMID: 26201776 2013 Hepatology international

Abstract: Importantly, less HBsAg was detected in the cells transfected with the rtA181T resistance mutants, and the overlapping sW172stop mutation ablated secretion of HBsAg into cell culture supernatants.

Abstract: We have recently shown that for HBV genotype D, the rtA181T/sW172stop substitution conferring resistance to adefovir dipivoxil (ADV) alters secretion of HBsAg and exerts a dominant-negative effect on wild-type virion secretion.

High frequency of complex mutational patterns in lamivudine resistant hepatitis B virus isolates.

PMID: 23408582 2013 Journal of medical virology

Abstract: Clonal analysis of these seven quasispecies even disclosed the presence of HBV isolates carrying further stop codons and in one case the occurrence of resistance mutation rtA181T without the stop codon mutation sW172*.

Hepatitis B e antigen-suppressing mutations enhance the replication efficiency of adefovir-resistant hepatitis B virus strains.

PMID: 23301549 2013 Journal of viral hepatitis

Abstract: HBV rtA181T mutants displayed abolished hepatitis B surface antigen (HBsAg) secretion, owing to a sW172* stop codon in the overlapping envelope gene.

Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation.

PMID: 23171829 2012 Virology journal

Result: After injection of the wild type (pHBV4.1) or the mutant (pHBVrtA181T/sW172*) plamids, the level of serum HBsAg in mice injected with the wild type plasmid was very high (OD>2.4) on day 1, 3, and 5, and became low (OD<0.2) since day 7.

Result: Compared to wild type, the rtA181T/sW172* mutant strain showed an approximately 0.8 log reduction on day 1, 2.6 log reduction on day 3, 1.5 log reduction on day 5, and 0.7 log reduction on day 7 in serum HBV DNA titers.

Result: However, the HBV DNA replication intermediates levels of the HBV mutant rtA181T/sW172* were detectable from day 1 to day 15 and p

Hepatitis B virus gene mutations in liver diseases: a report from New Delhi.

PMID: 22720023 2012 PloS one

Result: Among the patients of LC, SW172stop (6.4%) and SL173F (4.2%) mutations were also detected.

Discussion: A large percentage of the cases with rtA181T mutations developed SW172stop mutations.

Discussion: Drug resistant mutations to ADV have been reported mainly in the HBV polymerase domain D rtN236T or the domain B rtA181V/T, whereas a domain D rtN236T mutation does not overlap with the envelope gene, a mutation at rt

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: As observed in the baseline quasispecies, a significant portion of the 20 most frequent variants (highest average substitution frequencies in the 5 samples) led to stop codons (sW156*, sW172*, sW182*, sW191*, sW196* and sW199*), especially at LMV VBK and at the end of ADV, mainly due to mutation sW172*, related to rtA181T, (71.7% and 64%, respectively) and sW182*, rela

Hepatitis B virus rtA181T/sW172non-stop mutation may increase resistance fold to adefovir- and entecavir-resistant mutants compared to rtA181T/sW172* mutation.

PMID: 21933446 2011 BMC cancer

Abstract: BACKGROUND: Development of the hepatitis B virus (HBV) rtA181T/sW172* mutant could occur during prolonged lamivudine (LAM) therapy, conferring cross resistance to adefovir.

Abstract: CONCLUSIONS: Emergence of the rtA181T/sW172* mutant in LAM-resistant patients increased the risk of HCC development in the subsequent courses of antiviral therapy.

Introduction: Because of the overlap between the S and polymerase genes, a great proportion of patients carrying the rtA181T mutation also possessed the

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