Location: Virus and Prion ResearchTitle: E-PIG-enetic avenues: porcine mRNA and miRNA pathway analysis of highly pathogenic PRRSV infection
|FLEMING, DAMARIUS - OAK RIDGE INSTITUTE FOR SCIENCE AND EDUCATION (ORISE)|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/16/2019
Publication Date: 8/13/2019
Citation: Fleming, D.S., Miller, L.C. 2019. E-PIG-enetic avenues: porcine mRNA and miRNA pathway analysis of highly pathogenic PRRSV infection [abstract]. IVIS 2019 International Veterinary Immunology Symposium . p. 51.
Technical Abstract: BACKGROUND Studies of the host-pathogen interaction between pigs and highly pathogenic Porcine respiratory and reproductive syndrome virus (HP-PRRSV) have tried to uncover the process that allows the virus to evade the immune response to its benefit. The virus infects pigs through nasal passages, replicates within lung macrophages disrupting their normal function. Research has examined post-transcriptional expression, unfortunately, looking at differences in expression alone does not give information on the pathways and networks that are affected and that contribute to homeostatic imbalances due to infection. Therefore this study examined the effects mRNA and miRNA expression has on host biological networks. METHODS Analysis was carried using whole blood from both mock infected and HP-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 divided by dpi and used to examine biological networks targeted to be possibly 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 pro-inflammatory signaling may underlie the ability of HP-PRRSV to hinder homeostasis.