Shortly before exposure to (potential) infection the presence of sufficient exogenous type 1 IFN is expected to beneficially initiate an antiviral inflammatory response and an antiviral state [24, 25], while prolonged IFN therapy or the presence of IFN too late after viral exposure may enhance detrimental immunopathological effects causing lung tissue damage [31, 32].The potential of type 1 IFN to enhance ACE2 expression must also be considered [33, 34]. This evidence concerns the gene IFNA1 and infection.