Type I IFNs and pro-inflammatory cytokines are hardly expressed or appear late in cell-culture based models of CoV infection [147], and dysregulation of the IFN response is associated with severe lung immunopathology, influx of inflammatory monocyte-macrophages, and elevated levels of cytokines and chemokines in mouse models of SARS-CoV [141] and MERS-CoV [148] infection. This evidence concerns the gene IFNA1 and infection.