IFNAR2 and HIV infectious disease: Given limited cell and patient numbers combined with potential sampling biases, we caution that this observation requires much broader cohorts to validate a potential role for co-infections; still, we note our observation is suggestive of a role for chronic IFNs in the induction of ACE2, given that HIV infection is associated with persistent upregulation of ISGs, and we observed elevated amounts of IFNAR2, IFI30, and IKBKB (Utay and Douek, 2016) (FDR-adjusted p = 1.1E−6, 8.8E−9, 1.57E−7, respectively; HIV+ versus HIV− epithelial cells).