SUMO pathway, blood coagulation and oxidative stress in SARS-CoV-2 infection

Severe Acute Respiratory Syndrome Corona Virus 2 (SARS CoV-2) is currently an international pandemic causing coronavirus disease 19 (COVID-19). Viral entry requires ACE2 and transmembrane protease serine 2 (TMPRSS2) for membrane fusion or through endosomal pathway. This Study aims to assess transcriptomic changes and differentially expressed genes (DFGs) in COVID-19. METHODS: Transcriptomic data of the publicly available dataset (GSE147507) was quantile normalized and analysed for DFGs, network analysis and pathway analysis. RESULTS: DFG sets showed that 8 genes (SAE1, AEBP2, ATP1A1, DKK3, MAFF, NUDC, TRAP1, and VAV1) were significantly dysregulated in all studied groups. Functional analysis revealed that negative regulation of glucocorticoid biosynthesis, protein SUMOylation (SAE1), blood coagulation (VAV1) and cellular response to stress were affected by SARS CoV-2 infection. Cell line transduction with ACE2 vector didn't show significant changes in the dysregulated pathways. Also, no significant change was observed in expression levels of ACE2 or TMPRSS2 in response to SARS CoV-2 infection. Further analysis showed dysregulation of several genes in the SUMOylation pathway and blood coagulation process in human and cell lines transcriptome. Also, several Cathepsins proteases were significantly dysregulated in case of SARS CoV-2 infection. Genes related to cellular response to stress such as TRAP-1 and NOX were dysregulated in cases of SARS CoV-2 infection. CONCLUSION: Dysregulation in genes of protein SUMOylation, blood coagulation and response to oxidative stress pathways in SARS CoV-2 infection could be critical for disease progression. Drugs acting on SUMO pathway, VAV1, NOX genes could be studied for potential benefit to COVID-19 patients.