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Therefore, to elucidate how the SARS-CoV-2 infection affects the CFTR-dependent pro-inflammatory response, our approach was incubate SARS-CoV-2 or viral spike protein with otherwise normal lung epithelial cells, and to test for loss of CFTR and consequent activation of proinflammatory TNF/NFB signaling 40

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The mechanisms underlying this observed survival benefit could include the correction of abnormal cellular nucleotide, protein, and lipid synthesis