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?:abstract
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Coronavirus disease (COVID-19), caused by SARS-CoV-2, has affected over 65 million individuals and killed over 1.5 million persons (December 8, 2020; www.who.int)(1). While fatality rates are higher among the elderly and those with underlying comorbidities(2), host factors that promote susceptibility to SARS-CoV-2 infection and severe disease are poorly understood. Although individuals with certain autoimmune/inflammatory disorders show increased susceptibility to viral infections, there is incomplete knowledge of SARS-CoV-2 susceptibility in these diseases.(3–7) We report that the autoimmune PTPN2 risk variant rs1893217 promotes expression of the SARS-CoV-2 receptor, ACE2, and increases cellular entry mediated by SARS-CoV-2 spike protein. Elevated ACE2 expression and viral entry were mediated by increased JAK-STAT signalling, and were reversed by the JAK inhibitor, tofacitinib. Collectively, our findings uncover a novel risk biomarker for increased expression of the SARS-CoV-2 receptor and viral entry, and identify a clinically approved therapeutic agent to mitigate this risk.
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?:doi
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?:doi
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10.1101/2020.12.09.416586
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document_parses/pdf_json/c6a3d30655784076f1d25362e8e89ddf47993927.json; document_parses/pdf_json/aa948c4fae79d4279bca1e94d55248971ca1f74f.json
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document_parses/pmc_json/PMC7743066.xml.json
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BioRxiv; Medline; PMC; WHO
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Identification of a Novel Susceptibility Marker for SARS-CoV-2 Infection in Human Subjects and Risk Mitigation with a Clinically Approved JAK Inhibitor in Human/Mouse Cells
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