In contrast to the existing paradigm, SARS-CoV infection is successfully controlled and cleared in IFNAR1−/−, IFNGR−/−, IFNAGR−/− and IFNLR deficient mice while deletion of STAT1 leads to increased virus replication, morbidity and mortality following infection with either the human epidemic strain of SARS-CoV (Urbani) or a mouse adapted strain (rMA15). This evidence concerns the gene IFNAR1 and severe acute respiratory syndrome.