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 HBV mutation literature information.


  Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through Deregulated HIF1A, MGST2, and TGFbi.
 PMID: 32887289       2020       International journal of molecular sciences
Introduction: We investigated four such mutants (sL15*, sL21*, sW156*, and sW172*) in our 3TC-experienced HCC cases for their nearby locations to the transactivity-on-region, and proved sL15*, sL21*, and sW172* mutants to be oncogenic.


  Characterization of hepatitis B virus in Amerindian children and mothers from Amazonas State, Colombia.
 PMID: 29016603       2017       PloS one
Abstract: Two HBV escape mutants were identified, G145R, reported worldwide, and W156*; this stop codon was identified in a child with occult HBV infection.
Result: The second escape mutant identified had a change from guanine to adenine in nucleotide 621, which generated a stop codon in position 156 (W156*); this mutation was identified in sample 189_Tarapaca_AM (Accession number MF400842) obtained from a child with Occult HBV infection (OBI) (Table 2).
Discussion: The mutation, W156*, was identified in a sample obtained from a child having undergone the complete vaccination schedule.


  Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma.
 PMID: 24587012       2014       PloS one
Discussion: Among the 11 HBV S gene truncation mutants we have identified (sL15*, sL21*, sS61*, sC69*, sL95*, sW156*, sW163*, sW172*, sW182*, sW196*, and sL216*) in HBV-related  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


  Identification of nonsense mutations in hepatitis B virus S gene in patients with hepatocellular carcinoma developed after lamivudine therapy.
 PMID: 19430100       2009       Antiviral therapy
Abstract: NIH3T3 cells stably expressing sL21*, sW156* and sW172* pre-S/S mutants had increased tumourigenicity in nude mice.



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