![]() ![]() ![]() Our analysis highlights potential genetic factors contributing to inter-individual variation of SARS-CoV-2 infection and COVID-19 and suggests leads for mechanistic and translational studies. Several pSNVs associate with severe COVID-19 and hospitalization (STARD13, ARFGEF2). pSNVs disrupt CDK and MAPK substrate motifs and replace these with motifs of Tank Binding Kinase 1 (TBK1) involved in innate immune responses, indicating consistent rewiring of signaling networks. Proteins with pSNVs are involved in viral life cycle and host responses, including RNA splicing, interferon response (TRIM28), and glucose homeostasis (TBC1D4) with potential associations with COVID-19 comorbidities. We found 2,033 infrequent phosphorylation-associated SNVs (pSNVs) that are enriched in sequence motif alterations, potentially reflecting the evolution of signaling networks regulating host defenses. Here, we studied human missense single nucleotide variants (SNVs) altering phosphorylation sites modulated by SARS-CoV-2 infection, using machine learning to identify amino acid substitutions altering kinase-bound sequence motifs. ![]() Human genetic variation may impact SARS-CoV-2 infection and COVID-19 pathology however, the genetic variation in these signaling networks remains uncharacterized. SARS-CoV-2 infection hijacks signaling pathways and induces protein–protein interactions between human and viral proteins. ![]()
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January 2023
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