These observations supported the possibility of dysregulated IFN responsiveness among critically ill participants, which was unresolved in those who succumbed to infection, suggesting that higher viral loads could trigger elevated IFN signaling that may counterproductively turn on a negative feedback loop to suppress IFN signaling before the virus is cleared (62, 63) and contributing to mortality (Figure 6, B–E). This evidence concerns the gene IFNA1 and infection.