IL18R1 and severe acute respiratory syndrome: Unlike RSV and VSV, we found that WT C57BL/6 mice are protected from lethal SARS-CoV infection by a MyD88-dependent mechanism that does not involve adaptive immunity, the induction of type I/III interferon, or IL1-R/IL-18R signaling (data not shown) suggesting that SARS-CoV is interfacing with the innate immune system in a potentially novel manner.