Coronavirus infection elicits an immune response characterized by marked temporal phases and highly dynamic regulatory patterns, with the balance and subsequent disruption of cytokine signaling networks at its core. Through a diverse array of non-structural, structural, and accessory proteins, the virus rewires host immunity by suppressing interferon production, blocking JAK–STAT signalling, and activating NF-?B and MAPK pathways, thereby gaining a replicative advantage during the early stages of infection. A systematic delineation of the mechanisms underlying cytokine-signaling dysregulation will refine the immunopathological framework of coronavirus infection and inform more precise therapeutic strategies.