The antiviral activity of K83A mutant MxA protein against the replication of hepatitis B virus in vitro
Hui Li
Abstract
Hui Li
Abstract
Objective To investigate the antiviral activity of K83A mutant MxA protein against the replication of hepatitis B virus.Methods The recombinant vectors of pcDNA3.1-MxA(wild-type), pcDNA3.1-MxA(K83A)were cotransfected with PU19-1.24HBV repectively into HepG2 cells. After 3 dasys,the expression of MxA protein was detected by western blot. The supernatant HBsAg and HBeAg were measured by abbott analysis. HBV DNA was detected by real-time PCR.Results The MxA protein was expressed robustly in HepG2 cells of WT and K83A groups detected by western blot. Compared with the control group,the supernatant HBeAg in WT and K83A groups was decreased by 73% and 71%,the extracellular HBV DNA was decreased by 2.22 lg and 2.11 lg respectively and the intracellular HBV DNA was decreased by 1.89 lg and 1.78 lg respectively.Conclusion K83A mutation shows no influence on the interferon-inducible MxA protein to inhibit HBV replication.
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Objective To investigate the antiviral activity of K83A mutant MxA protein against the replication of hepatitis B virus.Methods The recombinant vectors of pcDNA3.1-MxA(wild-type), pcDNA3.1-MxA(K83A)were cotransfected with PU19-1.24HBV repectively into HepG2 cells. After 3 dasys,the expression of MxA protein was detected by western blot. The supernatant HBsAg and HBeAg were measured by abbott analysis. HBV DNA was detected by real-time PCR.Results The MxA protein was expressed robustly in HepG2 cells of WT and K83A groups detected by western blot. Compared with the control group,the supernatant HBeAg in WT and K83A groups was decreased by 73% and 71%,the extracellular HBV DNA was decreased by 2.22 lg and 2.11 lg respectively and the intracellular HBV DNA was decreased by 1.89 lg and 1.78 lg respectively.Conclusion K83A mutation shows no influence on the interferon-inducible MxA protein to inhibit HBV replication.
Key concepts: HBeAg, Hepatitis B virus, HBsAg, Western blot, Virology, Molecular biology, Mutant, Interferon