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

During HP-PRRSV infection, several aspects of the PAMs' function were under regulation, such as actin and tubulin cytoskeleton organization, exocytosis, protein degradation, protein folding, intracellular calcium and zinc homeostasis ( Table 3) . Increasing of intracellular zinc concentration impairs the replication of a variety of RNA viruses, including poliovirus, influenza virus, coronavirus, arterivirus, rhinovirus, and respiratory syncytial virus [40] [41] [42] . Recently, zinc ion has been reported to efficiently inhibit the RNA-synthesizing activity of the multiprotein replication and transcription complex of both SARS-coronavirus and equine arteritis virus [40] . Upregulation of SLC39A14 (also known as Zip14) (Table 3) , a member of the SLC39 (Zip) family which transports zinc from the extracellular space or organellar lumen into the cytoplasm [43] , might be a defense mechanism in PAMs during HP-PRRSV infection. Nevertheless, none of the SLC39 family genes was identified as a DE gene in a microarray assay of PAMs infected with PRRSV in vitro [8] . Furthermore, the expression of SLC39A7, another member of the SLC39 family, was downregulated in the lungs of Landrace×Yorkshire crossbred piglets at 7 dpi following HP-PRRSV infection [7] .