Influenza infection of IFNAR1−/−IL-28Rα−/− double knock-out epithelia induced the expression of IFNβ and IL-28A/B at levels comparable to the wild-type controls even at later time points during an infection (Fig. 5B), indicating that these genes are most likely upregulated directly downstream of the RIG-I/MAVS pathway and do not require IFN-driven positive feed-back on themselves. The gene discussed is IFNAR1; the disease is infection.