In addition, by using HepG2.2.15 cell line that stably expresses viral proteins and support HBV replication [19], we consistently found that IFN promoter activity induced upon SenV (Sendai virus) infection was pronouncedly diminished in HepG2.2.15 cells (Fig. 2D), validating the impact of HBV Pol in a more physiological setting. Here, IFNA1 is linked to viral infectious disease.