This lack of an effective antiviral response may be attributed to the immune response suppression mechanisms induced by IPNV, which allow for the establishment of a persistent infection, where an upregulation of anti-inflammatory cytokines, a downregulation of other pro-inflammatory cytokines, and even an increase in viral proteins that antagonize IFNa1 promoter activation and inhibit IFN-signaling has been described [29,31,66,67,68]. The gene discussed is IFNA1; the disease is infection.