Respiratory viruses establish primary infections in the nasal epithelium, where efficient induction of antiviral innate immunity may result in local control of viral replication, restriction of spread to the lower airway, and minimal pathogenesis. Human coronaviruses (HCoVs) cause a range of respiratory disease in their hosts – ranging from asymptomatic infections to mild upper respiratory symptoms to lethal pneumonia. However, the virus-host interactions that determine disease outcome are poorly understood. Innate immune antagonism by HCoVs is one factor that likely contributes to disease severity, optimizing viral replication and allowing for uninhibited spread to the lower airway. Middle East respiratory syndrome CoV (MERS-CoV) and severe acute respiratory syndrome-CoV-2 (SARS-CoV-2) are two lethal betacoronaviruses which encode various strategies to antagonize innate immune pathways induced following detection of double-stranded (ds)RNA by host sensors. Three dsRNA-induced pathways are investigated in this work: interferon (IFN) signaling, the protein kinase R (PKR) pathway, and the oligoadenylate ribonuclease (OAS/RNase L) pathway. Using recombinant viruses with inactivated antagonists of dsRNA-induced pathway, we find that MERS-CoV adeptly shuts down all three pathways via the combined activity of accessory proteins NS4a and NS4b, in addition to the conserved CoV endoribonuclease (nsp15 EndoU). Although SARS-CoV-2 modestly induces innate immune responses, inactivation of nsp15 EndoU during SARS-CoV-2 infection results in significantly increased IFN induction. We further find that inactivation of these viral antagonists confers attenuation of viral replication, which is rescued to wild-type levels when dsRNA-induced pathways were inhibited. We then leverage a primary nasal epithelial air-liquid interface (ALI) culture system to compare these lethal HCoVs with two common cold-associated HCoVs (HCoV-229E and HCoV-NL63), as well as a prototypical common cold picornavirus human rhinovirus-16 (HRV-16). We identify features of common cold-associated viruses in this system: optimal replication at nasal airway temperature (33ºC), robust and early induction of IFN signaling, and IFN-mediated clearance by nasal epithelial cells. We additionally highlight temperature dependent IFN responses as a broad mechanism of viral restriction. These findings highlight the importance of innate immune responses as well as viral antagonism of these responses as determinants of clinical disease severity during respiratory virus infections.