constructs we used the highly susceptible cell line HEK293 that also exhibits impaired IFNb-induced STAT1 phosphorylation at later stages of infection ( Figure 2E ). 24 h post transfection cells were stimulated with IFNb and STAT phosphorylation was monitored in Western blots (Figures 2A and C) . Expression of none of the viral proteins resulted in a significant decrease of IFNb-induced STAT1 or STAT2 phosphorylation (Figures 2A  and 2C ). Similar results were obtained in the human bronchial epithelial cell line H1299 when expressing M1, NS1 or NP alone or in different combinations (data not shown). Thus, we concluded that viral proteins most likely do not play a prominent role as blockers of IFNa/b-induced JAK/STAT signaling.