IFNA1 and viral infectious disease: The induction of type I and type III IFNs following viral infection is deficient in allergic asthmatic patients with poorly controlled asthma, either because of the strongly Th2-polarized environment at the respiratory mucosa and the use of corticosteroids that generically suppress IFN production and function (e.g., through the induction of SOCS1) or because of epigenetic changes that prevent optimal IFNλ gene expression and translation (31, 69, 70).