In the absence of IFN as an antiviral mechanism, the body activates an inflammatory response, which, especially in the lungs, has a pathogenic role: pulmonary edema, accumulation of monocytes/macrophages in the lung parenchyma, and secretion of pro-inflammatory cytokines (IL-1, IL-6) and chemokines (IP-10 = IFN induced protein 10, MIP1α, MIP1β, MIP-1 = monocyte attractant protein 1) attractive to monocytes, macrophages, and T lymphocytes at the site of infection. This evidence concerns the gene CCL3 and infection.