Molecular Characterization of Transcriptome-wide Interactions between Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus and Porcine Alveolar Macrophages in vivo

Zhou, Ping; Zhai, Shanli; Zhou, Xiang; Lin, Ping; Jiang, Tengfei; Hu, Xueying; Jiang, Yunbo; Wu, Bin; Zhang, Qingde; Xu, Xuewen; Li, Jin-ping; Liu, Bang

PRRSV is considered to inhibit the synthesis of type-I IFNs and its signaling by blocking STAT1/STAT2 nuclear translocation [35] . However, it is also reported that PRRSV can phosphorylate IFN-regulatory factor 3 (IRF-3) and weakly activate the IFN-β promoter in MARC-145 cells in early infection, but the activations of IRF-3 and IFN-β promoter are rapidly inhibited in the following infection [36] . The induction of IFN-β mRNA, but not IFN-α mRNA, is observed in monocyte-derived dendritic cells and primary alveolar macrophages infected by PRRSV at 12 dpi [8, 37] . In some cases, even the expression of IFN-α can be detected in the lung [38] or serum [39] of pigs infected with PRRSV during the early days. Interestingly, in this study, no induction of type-I IFN was detected in PAMs at 5 dpi (Figure 3) , whereas a series of IFN induced genes that are critical for the cell to defend itself against viral infection, were upregulated (Table 2) . Similar results were shown in lung tissues at 4 and 7 dpi following both PRRSV and HP-PRRSV infection [6, 7] , and it was speculated that the IFN induced genes were predominantly expressed by the uninfected cells [7] . Here, another possibility is suggested that a certain amount of type-I IFN might be induced at the early stage of the infection before 5 dpi.