ABSTRACT
Objective To analyze the impact of hepatitis B virus (HBV) replication and its coded X gene (HBx) expression on cell gene expression profile,especially the immune related gene expression level changes.Methods Overexpressed HBx gene was transiently transfected through lenti-virus and pcDNA3,the RNA-Seq and RT-qPCR methods were used to detect the expression levels of immune related genes,which were verified in HBV replication cell line.Results This study found that the HBV replication and HBx expression suppressed the expression of immune checkpoint PD-1 ligand gene (PD-L1/CD274) in a dose-dependent manner,while the expression of H-box mutant in HBx gene lost this inhibition effect.Conclusion HBV/HBx possesses the ability for inhibiting PD-L1/CD274 ligand gene expression,may relieve the checkpoint of antigen-specific T cell activation in viral infection acute stage,activates cytotoxic T cells,which may cause that T cell attack and clear highly replicated cells,helps virus to enter the lower replication status,and reaches the balance status between virus-host and lays a basis of HBV chronic infection.
ABSTRACT
Objective To analyze the impact of hepatitis B virus (HBV) replication and its coded X gene (HBx) expression on cell gene expression profile,especially the immune related gene expression level changes.Methods Overexpressed HBx gene was transiently transfected through lenti-virus and pcDNA3,the RNA-Seq and RT-qPCR methods were used to detect the expression levels of immune related genes,which were verified in HBV replication cell line.Results This study found that the HBV replication and HBx expression suppressed the expression of immune checkpoint PD-1 ligand gene (PD-L1/CD274) in a dose-dependent manner,while the expression of H-box mutant in HBx gene lost this inhibition effect.Conclusion HBV/HBx possesses the ability for inhibiting PD-L1/CD274 ligand gene expression,may relieve the checkpoint of antigen-specific T cell activation in viral infection acute stage,activates cytotoxic T cells,which may cause that T cell attack and clear highly replicated cells,helps virus to enter the lower replication status,and reaches the balance status between virus-host and lays a basis of HBV chronic infection.