Study On The Mechanism Of Promoting Hepatitis B Virus Replication By NOX2

ObjectionHepatitis B virus(HBV)is still a serious global public health issue that can cause chronic hepatitis,liver cirrhosis and hepatocellular carcinoma.NOX2,acted as a kind of NADPH oxidase,plays a critical role in various physiological and pathological processes.Our team previously found that serum NOX2 levels is significantly elevated in patients with CHB,and that the value of NOX2 is associated with the progress of diseases.However,the underlying mechanisms by which NOX2 affects HBV replication and expression remain unclear.This study aims to investigate the relationship between NOX2 and HBV replication in the cell models.Methods1.In the transiently and steady HBV-transfected cell models,the expression level of NOX2 was detected by Western blot,real-time PCR and immunofluorescence.2.In the transiently and steady HBV-transfected cell models,after inhibition of NOX2 enzymatic activity by chemical inhibitors,the changesof HBV core protein and mRNA levels,ROS production,and intracellular autophagy levels were measured.3.In the steady HBV-transfected cell models,after knocking down NOX2 levels by RNA interference,the changes of HBV core protein and mRNA levels,ROS production and intracellular autophagy levels were detected.4.In the steady HBV-transfected cell models,after overexpression of NOX2,the changes of HBV core protein and mRNA levels,ROS production and intracellular autophagy levels were detected.ResultsCompared with control group,NOX2 was highly expressed in the transiently and steady HBV-transfected cell models.After inhibition of NOX2 enzyme activity by chemical inhibitors and NOX2 knockdown,intracellular ROS levels were markedly reduced,and autophagy levels were also decreased,leading to inhibiting HBV replication and expression.After NOX2 overexpression,intracellular ROS levels were significantly elevated,and autophagy levels were up-regulated,resulting in an increase of HBV replication and expression.ConclusionHBV infection can facilitate the expression of NOX2.Elevated NOX2 promotes HBV replication and expression via mediated-ROS and autophagy.This suggests that HBV promotes its survival and infection inthe host through NOX2-ROS signaling pathway.