In addition to interfering with IFN production pathway, SARS-CoV has evolved multiple other mechanisms to modify host cell response. Viral RNA is unprotected and open to cellular degradation; however, some RNA viruses have evolved a capping process to evade recognition by the host. In SARS-CoV, Nsp16 provides ribose 2′-O-methylation at the 5′ end of the RNA to protect its degradation and prevent sensing by MDA5 (Züst et al., 2011). Similarly, Nsp14 had N7 methyltransferase activity and methylated the 5′ end of the RNA (Chen et al., 2009). Other SARS-CoV proteins involved include – Nsp4a, which prevents stress granule formation by inhibiting PKR mediated antiviral signaling (Rabouw et al., 2016). N protein of SARS-CoV-2 is also known to interact with the proteins implicated in stress granule regulation (Gordon et al., 2020). Electron tomography studies in SARS-CoV infected cells revealed a unique replication network derived from ER to organize viral replication while simultaneously hiding the viral RNA from recognition by host NASs (Knoops et al., 2008). Other RNA viruses have also developed similar strategies to evade sensing by forming double-membrane vesicles (DMVs) and replication organelles to prevent access to the NASs (Blanchard and Roingeard, 2015).