Because type I IFNs have been shown to be effective against SARS-CoV infection, both in vitro and in vivo[22], [23], [24], [25], [26], the deficient response of type I IFNs in infected hosts has led to the hypothesis that SARS-CoV has evolved strategies to evade this potent IFN-related innate antiviral response. This evidence concerns the gene IFNA1 and severe acute respiratory syndrome.