Type I IFN responses to PRRSV are likely to be severely inhibited when infection takes place through the antibody-dependent enhancement (ADE) pathway; following ADE, PRRSV is able to suppress the transcription of key antiviral genes such astumor necrosis factor-α (TNF-α) and interferon-β (IFN-β), which also implies the down-regulation of the genes coding for crucial transcription factors: interferon regulatory factor-1 (IRF-1), interferon regulatory factor-3 (IRF-3) and nuclear factor kappa B (NF-κB) [60]. The gene discussed is IRF1; the disease is infection.