Thus, despite a lower production of differentially expressed genes upon infection with huH1N1, the immune response was sufficient to control the infection with induction of important antiviral immune factors, such as the OAS family, the IFIT family, MX, ISG15, IFI6, RSAD2, BST2 etc. The infection with the swH1N1 virus induced a high number of antiviral genes, but the virus’ ability to still replicate efficiently might be due to a better capability to evade parts of the immune response, potentially through NS1 as proposed and/or a more abundant HA attachment (55, 56). Here, BST2 is linked to infection.