A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1.
Result: As anticipated, the levels of p53 and Smad4 that had been downregulated by the sW182* mutant were restored in the Jab1-depleted cells (Fig 4E and 4F).
Result: Based on the result of Fig 3, we examined the effect of the sW182* truncation mutant on the levels of Jab1 target tumor suppressors, p53 and Smad4.
Result: Each of these promoter activities was inhibited by the sW182* mutant (Fig 5A).
Result: Expression of th
Result: and we have recently reported that a nonsense mutant of LHBs, sW182* (Fig 1A), has an oncogenic potential, as nude mice xenografted with mouse embryonic fibroblasts (NIH3T3) transfected by the mutant showed strong tumorigenicity.
Molecular cloning and phenotypic analysis of drug-resistance mutants with relevant S-region variants of HBV for a patient during 189-month anti-HBV treatment.
Abstract: Further mutagenesis study revealed that the P5T mutation of core protein plays an important role in the enhanced viral replication through increasing the levels of capsid formation and pregenomic RNA encapsidation.
Result: After L97I reversion in the GYF isolate, the levels of pgRNA encapsidation, core DNA replication, and virion secretion, remained unchanged.
Result: Among those, I97L has been reported to be associated with the increased HBV DNA replication in Huh7 cells, we thus first examined the potential role of I97L in the replication fitness of GYF isolate.
Result: Considering that the P5T mutant did not completely bring up the WT replication to the level of GYF, it is plausible that
Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy.
PMID: 30906435
2019
Experimental and therapeutic medicine
Introduction: ADV-resistance has been associated with the rtN236T mutation in the D domain and/or the rtA181V/T mutation in the B domain.
Introduction: It has been indicated that LAM resistance is mostly associated with the rtM204I/V mutation in the tyrosine-methionine-aspartate-aspartate (YMDD) motif of the C domain of the polymerase gene.
Result: Common and frequent mutations identified in the cohort of the present study included rtL80V/I, rtV84M, rtL
Molecular and serological characterization of occult hepatitis B virus infection among patients with hemophilia.
Abstract: Sequencing revealed multiple substitutions in preS1, preS2, and S regions for one panel including a rare D144N substitution associated with vaccine breakthrough that emerged with increasing frequency as the breakthrough infection developed.
Result: However, the rtV207L substitution is associated with antiviral drug resistance.
Recombinant HBsAg of the Wild-Type and the G145R Escape Mutant, included in the New Multivalent Vaccine against Hepatitis B Virus, Dramatically Differ in their Effects on Leukocytes from Healthy Donors In Vitro.
Discussion: All results shown here confirm that HBx-B K130M/V131I mutant variant displayed a stronger tumorigenic effect than its wild-type counterpart.
Discussion: Taken together, these results provide a potential mechanism whereby HBV encoding X_K130M/V131I (BCP_A1762T/G1764A) may contribute to the high rate of HCC observed clinically in patient cohorts containing these mutations.
Discussion: The X_K130M/V131I amino acid changes are encoded by nucleotide changes at BCP
A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus.
Abstract: Among those with a viral load <=5.0 log IU/ml, patients with the G2765A substitution showed a significantly lower HBV viral load than those with the wild-type sequence.
Abstract: CONCLUSION: G2765A substitution in the pre-S1 promoter reduced the expression of L protein and resulted in a low viral load and less severe disease in Method: The mutation vectors were constructed by the inverse PCR method using primer m5 (G2765A), a sense primer for the G-to-A substitution at the third nucleotide of the Sp1 region, and primer m9 (whole nucleotide mutation), a sense primer for a whole nucleotide mutation of the Sp1 region, and antisense primer mR (Table 1).
Analysis of hepatitis B virus genotype and gene mutation in patients with advanced liver disease in East Kalimantan, Indonesia.
Abstract: The C1505A mutation in X region, T1753V and A1762T/G1764A mutations in the basal core promoter region and C1858T in precore (PC) region were frequent and only detected in patients with ALD (28.9, 40, 73.5 and 17.6%, respectively), whereas the G1896A mutation in the PC region was frequently detected in HBV carriers.
HBV mutation literature information.
PMID: 
2019
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