In these cells, diminished IFN-β expression prior to infection (and early after infection, see below) allows the virus a head start, and even though IFN-β production eventually catches up to (and even exceeds) wild-type levels, the temporal advantage conferred to the actively replicating RNA viruses during an acute infection ultimately proves insurmountable [16], [19]. This evidence concerns the gene IFNB1 and infection.