Location: Virus and Prion ResearchTitle: Comparative analysis of signature genes in PRRSV-infected porcine monocyte-derived cells to different stimuli
|FLEMING, DAMARIUS - Orise Fellow|
|LI, XIANGDONG - Collaborator|
|BLECHA, FRANK - Kansas State University|
|SANG, YONGMING - Tennessee State University|
Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 9/19/2017
Publication Date: 12/3/2017
Citation: Miller, L.C., Fleming, D., Li, X., Bayles, D., Blecha, F., Sang, Y. 2017. Comparative analysis of signature genes in PRRSV-infected porcine monocyte-derived cells to different stimuli. 98th Conference of Research Workers in Animal Diseases. Abstract No. 237, p. 131.
Technical Abstract: Monocyte-derived DCs (mDCs) are major target cells in porcine reproductive and respiratory syndrome virus (PRRSV) pathogenesis; however, the plasticity of mDCs in response to activation stimuli and PRRSV infection remains unstudied. In this study, we polarized mDCs, and applied genome-wide transcriptomic analysis and predicted protein-protein interaction networks to compare signature genes involved in mDCs activation and response to PRRSV infection. Porcine mDCs were polarized with mediators for 30 hours, then mock-infected, infected with PRRSV strain VR2332, or a highly pathogenic PRRSV strain (rJXwn06), for 5 h. Total RNA was extracted and used to construct sequencing libraries for RNA-Seq. Comparisons were made between each polarized and unpolarized group (i.e. mediator vs. PBS), and between PRRSV-infected and uninfected cells stimulated with the same mediator. Differentially expressed genes (DEG) from the comparisons were used for prediction of interaction networks affected by the viruses and mediators. The results showed that PRRSV infection inhibited M1-prone immune activity, downregulated genes, predicted network interactions related to cellular integrity, and inflammatory signaling in favor of M2 activity. Additionally, the number of DEG and predicted network interactions stimulated in HP-PRRSV infected mDCs was superior to the VR-2332 infected mDCs and conformed with HP-PRRSV pathogenicity.