In RSV, influenza, and CoV-2-infected experimental mouse models of acute innate inflammation and also in humans, this transition is characterized by excessive neutrophil influx, activation of macrophages, and exacerbated expression of type CC, CXC chemokines (IL-8, monocyte chemoattractant protein-1 (MCP-1 or CCL2), macrophage inflammatory protein-1 (MIP-1 or CCL3), cytokines (e.g., TNF-α), interleukins (IL-1β, IL-6), interferons (INFγ, IFNα and INFλ), and growth factors (e.g., granulocyte colony-stimulating factor, G-CSF). Here, CSF3 is linked to influenza.