Indeed, we observed that the most considerable augmentation of pro-inflammatory IL-1β, IL-6, IL-15, IL-18, IFN-γ, eotaxin, GRO-α, IP-10, MCP-1, MIP-1α, MIP-1β, and regulatory IL-1RA, occurred at the terminal stage of the disease (7 days post-infection) in our rhesus macaques. The gene discussed is IL1B; the disease is infection.