Following infection, PRRSV poorly induces innate immune responses, e.g., phagocytic and microbicidal activities, Ag presentation and T-cell activation, expression of pattern recognition receptors [e.g., Toll-like receptor 3 (TLR3) and TLR7], production of type I and II interferons (IFN), and production of pro-inflammatory cytokines [e.g., interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFα)] (5–7). This evidence concerns the gene TNF and infection.