Both SARS-CoV and SARS-CoV-2 have evolved multiple inhibitory mechanisms to evade host cell recognition. Inhibition of host transcriptional and translational machinery prevents the biosynthesis of protective IFNs and delays early activation of host cell apoptosis. Nsp1 of SARS-CoV inhibit the loading of ribosomal 40s subunit and prevent host cell protein translation. Further, Nsp1 specifically degrade host cell RNA while sparing the viral RNA (Huang et al., 2011; Tanaka et al., 2012; Lokugamage et al., 2015). N protein of SARS-CoV-2 also interacts with the host biosynthetic protein La-related protein 1 (LARP1). This interaction may serve as the necessary signal to shut down the host cell protein synthesis for the propagation of SARS-CoV-2 (Gordon et al., 2020).