Our results and previous studies indicated that during the early stage of SARS-CoV-2 infection, especially in severe adult COVID-19 patients, type I interferon response including IFN-α production and activity is markedly suppressed, which in turn facilitates persistent viral replication, excessive proinflammatory cytokine production, and systemic inflammation (Hadjadj et al., 2020), although excessive type I IFN response is a well-documented factor that can worsen COVID-19 by promoting hyperinflammation (Lee et al., 2020). This evidence concerns the gene IFNA1 and COVID-19.