Papain-like protease of SARS-CoV directly interacts with p53 and induce its degradation, which may thus interfere with translation and delay early apoptosis of the infected cells (Yuan et al., 2015; Ma-Lauer et al., 2016). SARS-CoV S protein also interacts with the translation initiation factor eIF3f and inhibit host cell translation by preventing its nuclear import (Xiao et al., 2008). Studies from other respiratory viruses have shown that cells which activate early apoptosis prevent further spread of the viruses, whereas viruses that successfully inhibit this pathway exhibit strong infectivity (Orzalli and Kagan, 2017). Cytomegaloviruses (CMVs) distinctly rely on this mechanism to successfully replicate within the host cell by inhibiting apoptosis-modulatory proteins such as Bax and Bcl-2 (Çam et al., 2010). However, whether SARS-CoV or SARS-CoV-2 are also directly involved in inhibiting early apoptosis remains to be tested, but it is evident that these viruses induce host cell death after successful propagation and dissemination.