All PRRSV-2 strains exhibited moderate pathogenicity without mortality, following a similar infection course characterized by interstitial pneumonia, cytokine cascades (e.g., IFN-α, IFN-γ, IL-1β, IL-12p40, IL-10, CCL2, CCL5, CCL8, and CXCL10), and upregulation of interferon-stimulated genes [e.g., ISG12(A)]. Here, CCL8 is linked to infection.