Given that pulmonary epithelial cells (ECs) are the primary target for SARS-CoV-2 infection3–5 and that IFNγR-deficient ECs in the presence of an IFNγR-sufficient immune compartment still have increased viral loads, we propose that bacteria-induced IFNγ likely mediates its anti-viral effects directly within EC. This evidence concerns the gene IFNG and COVID-19.