We speculate that NS1 mutations that confer decreased IFN-β induction in the mouse lung may in some cases allow replication to higher titres before inhibitory levels of IFN are reached, ultimately resulting in greater spread and infection in the lung and correspondingly, increased disease severity and mortality (as seen for the majority of mutant NS1 genes) (Fig. 2, 3, Table 1). This evidence concerns the gene IFNA1 and infection.