Here, the discordant kinetics for viral clearance and pathogen-initiated inflammatory responses are indicative of an excessive and prolonged induction of genes for viral host defense that persisted long after their essential roles in viral clearance and suggest a risk window of adaptive homeostasis, where intervention with proresolving mediators that dampen IFN signaling could mitigate post-IAV risk for secondary bacterial infection. Here, IFNA1 is linked to bacterial infectious disease.