STAT2 and infection: To further confirm that the increased infection rate by the adapted viral population is independent from the early ISG response, we compared the viral replication kinetics in both human U6A cells deficient for STAT2 (i.e., an ISG transcription regulator of the signaling pathway induced by IFN-I and III), and U6A cells complemented for STAT2 expression, referred to as STAT2-U6A cells (Fig. 2f, upper panels).