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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #338858
Research Project: Intervention Strategies to Control Endemic and New and Emerging Viral Diseases of Swine

Location: Virus and Prion Research

Title: Transcriptomic analysis reveals the potential of highly pathogenic PRRS virus to modulate immune system activation related to host-pathogen and damage associated signaling in infected porcine monocytes

Author
item Miller, Laura
item FLEMING, DAMARIUS - Orise Fellow
item LI, XIANGDONG - Collaborator
item Bayles, Darrell
item BLECHA, FRANK - Kansas State University
item SANG, YONGMING - Tennessee State University

Submitted to: International Society for Animal Genetics Conference
Publication Type: Abstract Only
Publication Acceptance Date: 3/16/2017
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: One of the largest risks to the continued stability of the swine industry is by pathogens like porcine reproductive and respiratory syndrome virus (PRRSV) that can decimate production as it spreads among individuals. These infections can be low or highly pathogenic, and because it infects monocytic cells, PRRSV can undermine the innate immune response. This is especially true of the interferon stimulated inflammatory response. To shed light on the effect of PRRSV pathogenicity on activation status of the immune response, we polarized infected and control monocyte-derived cells (mDCs), applied transcriptomic analysis, and predicted protein-protein interactions as networks to elucidate the interconnected biological processes related to low and highly pathogenic PRRSV infection. Differentially expressed genes (DEGs) from each polarized/unpolarized and PRRSV infected/ uninfected comparison was used to predict networks and subsequent molecular functions affected by the viruses and mediators. The analysis uncovered previously uncharacterized evidence of the ability of PRRSV to affect M1 activation by altering expression of genes related to viral defense, the extra-cellular matrix (ECM), toll-like receptor (TLR) signaling, and damage induced inflammatory signaling. Genes showing variability in expression, as well as the most common predicted biological network from the comparisons, were related to cellular structure and inflammatory immune responses. These results supply additional insight into the interplay of PRRSV pathogenicity and immune system evasion by affecting multiple routes of host inflammatory signaling, as well as mDC polarization.