Location: Virus and Prion ResearchTitle: Porcine messenger RNA and microRNA pathway analysis of PRRSV infection
|MILLER, LAURA - US Department Of Agriculture (USDA)|
|FLEMMING, DAMARIUS - Oak Ridge Institute For Science And Education (ORISE)|
Submitted to: Journal of Immunology
Publication Type: Proceedings
Publication Acceptance Date: 2/4/2020
Publication Date: 5/1/2020
Citation: Miller, L.C., Flemming, D.S. 2020. Porcine messenger RNA and microRNA pathway analysis of PRRSV infection. In: Proceedings of Journal of Immunology. May 8-12, 2020, Honolulu, Hawaii. 204(1 Supplement)92.14.
Technical Abstract: Porcine messenger RNA and microRNA pathway analysis of Porcine Reproductive and Respiratory Syndrome Virus infection Laura C Miller1 and Damarius Fleming1,2 1USDA-ARS Natl. Animal Dis. Ctr., 2ORAU OBJECTIVE Studies of the host-pathogen interaction between pigs and porcine respiratory and reproductive syndrome virus (PRRSV) have tried to uncover the process that allows the virus to evade the immune response to its benefit. This study examined the effects messenger RNA (mRNA) and microRNA (miRNA) expression has on host biological networks. METHODS Analysis was carried using whole blood from both mock infected and PRRSV infected pigs. Transcriptomic techniques were then applied to examine the differential expression of miRNAs using Hisat2 for alignment to the Sus scrofa 10.2 genome and changes in expression analyzed using DeSeq2. Statistical significance for pathway analysis was set at FDR = 0.5. The resulting list of miRNAs were examined for their effects on porcine biological networks using the mirPATH software to generate KEGG pathways affected by changes in miRNA differential expression. RESULTS The results of the statistically significant (FDR = 0.15) miRNAs were defined by days post inoculation (dpi) to examine biological networks inhibited or activated by the identified miRNAs. Post-transcriptional control of host gene expression appeared to take place over several host biological pathway groupings which effect homeostasis that included immune, metabolic, and structural pathways. This included pathways such as the proteoglycan in cancer pathways that showed multiple genes targeted for inhibition that would cause host dysregulation and impair the ability to properly maintain homeostasis during infection. CONCLUSION The analyses suggests inhibition and activation of networks involved in viral entry, proliferation, and proinflammatory signaling may underlie the ability of PRRSV to hinder homeostasis.