IFNA1 and COVID-19: An imbalanced host response to SARS-CoV-2 drives the development of COVID-19, as SARS-CoV-2 infection hampers IFN production and weakens antiviral defenses, but concomitantly promotes an exacerbated production of cytokines (“cytokine storm”) and profibrotic factors, and enhanced recruitment and accumulation of leukocytes in tissues causing ARDS (2, 3).