The anti-IFN action of NS1 is exerted through a combination of several possible NS1-host cell interactions, such as: (i) down-regulation of new cellular transcription elongation and post-transcriptional RNA processing after infection [40]–[42], (ii) inhibition of RIG-I activation [21]–[23], [43], (iii) interference with the IFN signaling [44], [45] and (iv) direct inhibition of specific ISGs, like PKR and RNAse L [46]–[48]. Here, IFNA1 is linked to infection.