The upregulated expression of type II interferon receptors (IFNAR1 and IFNAR2) in CD4+ TCM and classical monocytes were more pronounced in active COVID-19 groups compared to recovered, where type I interferon receptor (IFNGR1 and IFNGR2) expression dominated, thereby suggesting a surge of proinflammatory cytokines mediated via type II IFN receptor signaling during the active COVID-19 disease. Here, IFNGR1 is linked to COVID-19.