Designed Artificial Transcription Factors Inhibit Hepatitis B Virus Transcription in HepG2.2.15 Cells

Hepatitis B virus (HBV) causes serious health issues worldwide. Despite this, current treatment options for HBV have many drawbacks. Strategies to safely and specifically target HBV replication and survival at the transcriptional level within host cells arc needed to combat current drawbacks in treatment. In this study, we designed a novel artificial transcription factor (ATF) with suppressive function to target and bind to the HBV core promoter, a component that plays a central role in the viral life cycle. ATF has attached specifically to the intended target site by using electrophoretic mobility shift assays (EMSA). We tested whether targeting this suppressive ATF had any effect on HBV gene expression by transfection factor, western blotting, and real-time PCR. In the presence of ATF, viral mRNA and DNA levels were significantly decreased within HepG2.2.15 cells compared to control cells. The HBV-derived protein expression of HBV-e antigen (HBeAg) and HBV-c antigen (HBcAg) was also significantly inhibited. These results show that ATF treatment targeting the HBV core protein promoter has an antiviral effect and inhibits HBV infection in host cells. These results further suggest that the design of new artificial transcription factors may be valuable antiviral therapies to treat HBV patients.