ISG12a inhibits HCV replication and potentiates the anti-HCV activity of IFN-α through activation of the Jak/STAT signaling pathway independent of autophagy and apoptosis
Overexpression of ISG12a inhibited HCV RNA replication both in Con1b replicon and the HCV JFH1-based cell culture system. ISG12a promoted the production of IFN α/β and activated the type I IFN signaling pathway. ISG12a potentiated the anti-HCV activity of IFN-α.