This COVID‑19 event has been created by a combination of computational inference from SARS-CoV-1 data (https://reactome.org/documentation/inferred-events) and manual curation, as described in the summation for the overall SARS-CoV-2 infection pathway.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).
Maier, HJ, Vaux, LC, Gerner, W, Wileman, T, Ktistakis, NT, Manifava, M, Chandra-Schoenfelder, P, Britton, P, Cottam, EM
Abu-Asab, M, Shi, CS, Kehrl, JH, Huang, NN, Shelhamer, JH, Qi, HY, Boularan, C
McAuliffe, J, Prentice, E, Lu, X, Denison, MR, Subbarao, K
Shi, CS, Kehrl, JH, Huang, NN, Nabar, NR
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