The marked reductions in type I IFN responses to viral stimuli reported herein in males, coupled with the relationships with virus-induced exacerbations of lung disease, and with severe viral LRTIs among male participants and among those with the most deficient IFN induction in our cohort, indicate that the deficient IFN responses we report in males may be in part responsible for the adverse outcomes to SARS-CoV-2 infection currently being reported in males. The gene discussed is IFNA1; the disease is lung disorder.