Preceding studies on human infecting coronaviruses (CoVs) have demonstrated a critical role of nucleic acid-sensing (NAS) pathways in recognizing various components of these viruses to initiate an early antiviral response. Whereas, potent inhibitory mechanisms are developed by CoVs to prevent or delay early antiviral responses (Rose et al., 2010; Adedeji et al., 2013). These inhibitory signals affect a range of host defense pathways to allow the propagation of CoVs. Some inhibitory signals may even activate cell death pathway to induce a robust proinflammatory state. Studies from in vitro cell culture, animal models, and patients who have successfully recovered from SARS-CoV infection have provided detailed molecular insights about signaling molecules implicated in virus-host interaction that may also serve as a model to understand a similar process in SARS-CoV-2 (Totura and Baric, 2012).