These results indicate that the regulations of cellular antiviral immune responses and inflammatory responses mediated by NF-κB, JAK/STAT, MAPK, and NLRP3 pathways, contribute to immune escape of PCV2 and PRV and host antiviral responses, which may be of great value for the research and control of infection and related diseases of PCV2 and PRV. The gene discussed is SOAT1; the disease is infection.