Porcine reproductive and respiratory syndrome virus counteracts type I interferon-induced early antiviral state by interfering IRF7 activity.

Porcine reproductive and respiratory syndrome (PRRS) is an economically important disease with a significant impact on the pig industry. It is caused by PRRS virus (PRRSV), which predominantly infects and replicates in porcine pulmonary alveolar macrophages (PAMs). We pretreated PAMs with porcine interferon (IFN)-α to induce an antiviral state within the cells and subsequently infected them with highly pathogenic PRRSV. Changes in global gene expression in IFN-α-pretreated PAMs in response to PRRSV infection were determined by RNA-sequence analysis and confirmed by real-time PCR. We found that IRF7 and other antiviral interferon stimulating genes (ISG)s were suppressed by PRRSV infection. Further studies demonstrated that PRRSV could down-regulate the expression of IRF7 by the non-structure protein 7 (nsp7). In conclusion, PRRSV infection had a strong immunosuppressive effect of IFN. PRRSV nsp7 inhibits the expression of IRF7, thereby down-regulating the expression of IFN and downstream ISGs and facilitated the virus to replicate.