In summary, we demonstrated that human bronchial epithelial 2B4 cells are capable of responding to SARS-CoV infection by temporally activating latent NFκB (12-hrs), AP-1 (ATF2/-Jun) (24-hrs), and IRF-3/7 (48-hrs), all of which, especially IRF-3/7, are critically involved in the induction of type I IFN gene expression and the subsequent activation of virus-dependent and/or IFN-dependent antiviral signaling pathways. Here, JUN is linked to severe acute respiratory syndrome.