The replicase polyprotein 1a of the human severe acute respiratory syndrome coronavirus (SARS-CoV) is post-translationally cleaved by virally encoded proteases to generate non-structural proteins (nsps). Viral nsps induce the formation of ER-bound double membrane vesicles (DMV) in host cells post infection. These DMVs are decorated with Microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B) proteins that are involved in autophagosome formation. However, there is no evidence that DMVs are recruited to the autophagy machinery. Studies show that nsp6 localize in the endoplasmic reticulum and induces the translocation of MAP1LC3B to the autophagosomes (Cottam E M. et al 2011). It is known that non-structural proteins (nsp) in SARS-CoV viruses induce the formation of ER-bound double membrane vesicles (DMV) in host cells post infection. These DMVs are decorated with Microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B) proteins that are involved in autophagosome formation. However, there is no evidence that DMVs are recruited to the autophagy machinery. Studies show that sars8b (8b) can trigger cellular stress, which results in a calcineurin dependent Transcription Factor EB (TFEB) activation and its target genes. This leads to an increase in autophagic flux (Shi C S. et al 2019). The replicase polyprotein 1a of the human severe acute respiratory syndrome coronavirus (SARS-CoV) is post-translationally cleaved by virally encoded proteases to generate non-structural proteins (nsps). Viral nsps induce the formation of ER-bound double membrane vesicles (DMV) in host cells post infection. These DMVs are decorated with microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B) proteins that are involved in autophagosome formation. However, there is no evidence that DMVs are recruited to the autophagy machinery. Immunofluorescence studies show that nsp6 (Cottam E M. et al 2011) and nsp8 (Prentice E. et al 2004) colocalizes with MAP1LC3B suggesting a binding event. In some cell types, expression of sars9b (9b) triggers the formation of autophagosomes and underlying molecular mechanisms are unclear (Shi C S. et al 2014). Studies also show that sars8b (8b) can trigger cellular stress, which results in a calcineurin dependent Transcription Factor EB (TFEB) activation and its target genes. This leads to an increase in autophagic flux (Shi C S. et al 2019). It is known that non-structural proteins (nsp) in SARS-CoV viruses induce the formation of ER-bound double membrane vesicles (DMV) in host cells post infection. These DMVs are decorated with Microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B) proteins that are involved in autophagosome formation. However, there is no evidence that DMVs are recruited to the autophagy machinery. In some cell types, expression of sars9b (9b) triggers the formation of autophagosomes and underlying molecular mechanisms are unclear (Shi C S. et al 2014).