IFNA1 and COVID-19: At the molecular level, hyper-regulation of pro-inflammatory mediators (including IL-6, TNFα, S100A8/9, and C-reactive protein), a significant decrease of human leukocyte antigen D-related (HLA-DR) gene expression in CD14 monocytes, and dysregulated antiviral interferon (IFN) response have been reported in COVID-19 patients with critical illness [13,14,15].