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

In macrophages, PRRSV entry into the host cell is mediated by heparan sulphate proteoglycans and the receptor sialoadhesin. Upon a pH drop, PRRSV is uncoated and its genome is released from the endosomes into the cytoplasm, which allows virus replication [22] . After HP-PRRSV infection the ATP6V1B2 gene, which encodes a component of vacuolar ATPase (V-ATPase) that mediates acidification of endosomal organelles [23] , was upregulated ( Figure 3 ). SARM1, a negative regulator of TRIF-dependent Toll-like receptor (TLR) signaling [24] and MAPK phosphorylation [25] , was significantly downregulated (Figure 3 ). SBNO2, a potent inhibitor of NF-κB [26] , and SOCS1 which limits NF-κB signaling by decreasing p65 stability within the cell nucleus [27] , were upregulated ( Figure 3 ). Upon HP-PRRSV infection, IRF7 was found to be upregulated in PAMs at 5 dpi ( Figure 3) , however, no type-I IFN or IFN-γ induction was observed. A number of IFN-induced genes (IFI6, IFI16, IFIH1, IFIT2, IFIT3, IFITM3, GBP1, GBP2, MX1, GZMB, GZMH, ISG15, USP18, RSAD2, NMI) were upregulated (Table 2) . JAK-STAT pathway seemed to be positively (STAT1 and NMI) as well as negatively (SOCS1) regulated during HP-PRRSV infection (Figure 3 ).