Selected article for: "complement system and intracellular zinc homeostasis"

Author: 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
Title: Molecular Characterization of Transcriptome-wide Interactions between Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus and Porcine Alveolar Macrophages in vivo
  • Document date: 2011_8_7
  • ID: js7l86fh_40
    Snippet: In summary, the data presented in this study suggested that during infection with HP-PRRSV Tongcheng piglets exhibited typical clinical signs, but displayed mild regional lung damage at 5 and 7 dpi. Microarray analysis revealed that HP-PRRSV infection has affected PAMs in vivo in expression of the important genes involved in cytoskeleton and exocytosis organization, protein degradation and folding, intracellular calcium and zinc homeostasis. Seve.....
    Document: In summary, the data presented in this study suggested that during infection with HP-PRRSV Tongcheng piglets exhibited typical clinical signs, but displayed mild regional lung damage at 5 and 7 dpi. Microarray analysis revealed that HP-PRRSV infection has affected PAMs in vivo in expression of the important genes involved in cytoskeleton and exocytosis organization, protein degradation and folding, intracellular calcium and zinc homeostasis. Several potential antiviral strategies might be employed in PAMs, including upregulating IFN-induced genes and increasing intracellular zinc ion concentration. Furthermore, inhibition of the complement system likely attenuated the lung damage during HP-PRRSV infection. This system analysis could lead to a better understanding of the HP-PRRSV-host interaction, and to the identification of novel antiviral therapies and identifying genetic components for swine tolerance/susceptibility to HP-PRRS.

    Search related documents:
    Co phrase search for related documents
    • antiviral therapy and clinical sign: 1
    • antiviral therapy and complement system: 1, 2
    • antiviral therapy and IFN induce: 1, 2
    • antiviral therapy and important gene: 1, 2
    • complement system and HP prrsv: 1, 2, 3
    • complement system and HP PRRSV host: 1
    • complement system and HP PRRSV host interaction: 1
    • complement system and HP prrsv infection: 1, 2, 3
    • complement system and HP prrsv infection lung damage: 1, 2
    • complement system and important gene: 1, 2
    • complement system and intracellular calcium: 1
    • complement system inhibition and HP prrsv: 1, 2
    • complement system inhibition and HP PRRSV host: 1
    • complement system inhibition and HP PRRSV host interaction: 1
    • complement system inhibition and HP prrsv infection: 1, 2
    • complement system inhibition and HP prrsv infection lung damage: 1, 2
    • complement system inhibition and intracellular calcium: 1
    • HP prrsv and IFN induce: 1
    • HP prrsv and important gene: 1