By Dr. Sanchari Sinha Dutta, Ph.D.Oct 26 2022Reviewed by Benedette Cuffari, M.Sc. A recent iScience study finds that the swine acute diarrhea syndrome coronavirus promotes autophagy to maintain its replication inside host cells. More specifically, the virus downregulates AKT/ mammalian target of rapamycin pathway to induce autophagy.
SADS-CoV is a bat-origin zoonotic coronavirus that was recently discovered in 2017. The virus exhibits potential cross-species transmissibility and is capable of infecting a range of cells derived from pigs, rats, monkeys, and humans. This highlights the need for understanding its host-pathogen interactions to identify potential antiviral therapeutics.
Impact of SADS-CoV infection on autophagy Cells derived from monkeys and pigs were infected with SADS-CoV-2 and subjected to autophagy analysis at various time points. The modulation of autophagy was assessed by estimating the expression of a vital autophagosome marker LC3-II. Related StoriesThe impact of autophagy on SADS-CoV replication was assessed by using rapamycin and 3-metyhlademine, which is a well-established inducer and inhibitor of autophagy, respectively. While rapamycin was found to induce both autophagy and viral replication in host cells, an opposite effect was observed in cells treated with 3-methylademine.
A series of experiments conducted to determine the mechanistic details of SADS-CoV-induced autophagy indicated that the virus induces complete autophagic flux to promote its replication. Inhibition of autophagosome-lysosome fusion was found to disrupt viral replication. Impact of autophagy inhibition on SADS-CoV replication The proteomics analysis of SADS-CoV-infected cells was conducted to identify potential antiviral target molecules. This led to the identification of eight differentially expressed proteins related to the PI3K/AKT pathway. Of these proteins, only integrin α3 exhibited antiviral effects against SADS-CoV replication.
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