Role of SARS-CoV-2-mediated Type I IFN antagonism in individuals with Down Syndrome

Down syndrome is principally caused by trisomy of chromosome 21, resulting in extra copies of the interferon receptors, IFNAR1 and IFNAR2. Signaling through these IFN receptors to initiates the highly potent antiviral and inflammatory functions of the type I Interferons (IFNs) response. The purpose of this study is to understand how altered IFN receptor availability, as is the case in Downs syndrome individuals, impact the SARS-CoV-2 pathogenesis.