[Tetracycline-inducible replications of wild-type and an adefovir-dipivoxil-resistant hepatitis B virus in human liver cells].
PMID: 27029368
2016
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
Abstract: After stable transfection of the HBV constructs into HepG2-off23 cells, cell lines with robust and tetracycline-inducible replications of wild-type HBV (HepG2-tetHBV-WT) and rtE218G-mutated HBV (HepG2-tetHBV-E218G) were selected.
Abstract: CONCLUSION: Wild-type and the rtE218G HBV mutant could be expressed and efficiently regulated by tetracycline in the established new cell lines.
Abstract: HBV mutant with rtE218G could independently confer resistance to adefovir in vitro.
Abstract: IC50 for HBV rtE218G mutant of adefovir was (6.49+-0.09) mumol/L, which was significantly higher than that for wild type virus (2.49+-0.05) mumol/L.
Abstract: M
rtE218G, a novel hepatitis B virus mutation with resistance to adefovir dipivoxil in patients with chronic hepatitis B.
Abstract: RtE218G-mutated HBV also showed a decreased replication capacity in vitro, equal to 87% of wild-type HBV.
Abstract: Phenotypic analyses demonstrated that the rtE218G mutation could independently confer resistance to ADV in vitro, with a 50% inhibitory concentration (IC(50)) 5.5-fold higher than wild-type HBV.
Abstract: The present study showed that the rtE218G mutation may be a novel ADV-resistant mutation.
Abstract: This mutant exhibited a substitution of glycine for glutamic acid at residue 218 (rtE218G).
Abstract: Transient transfection of the HBV replication-competent construct including the rt