Location: Virus and Prion ResearchTitle: Host response in the porcine thymus to PRRSV 2 and Influenza B coinfection
|SARLO DAVILA, KAITLYN - Oak Ridge Institute For Science And Education (ORISE)|
|SANG, YONGMING - Tennessee State University|
|MA, WENJUN - University Of Missouri|
Submitted to: Plant and Animal Genome Conference
Publication Type: Abstract Only
Publication Acceptance Date: 12/29/2021
Publication Date: 1/8/2022
Citation: Sarlo Davila, K.M., Sang, Y., Ma, W., Miller, L.C. 2022. Host response in the porcine thymus to PRRSV 2 and Influenza B coinfection. Plant and Animal Genome Conference. CRWAD Conference Proceedings.
Technical Abstract: Both Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) and influenza B (IBV) cause natural infections in pigs. PRRSV is the more common swine infection and can develop coinfections with IBV, a zoonotic virus able to infect humans. As a primary infection PRRSV can suppress the host immune system, leaving pigs susceptible to secondary infections such as IBV and contributing to the enormous economic impact of the disease. One component of this immunosuppression is the ability of PRRSV to affect the thymus and impair its normal function. This study investigates the host transcriptomic response in the thymus following PRRSV and IBV infections as well as their coinfection. Seronegative pigs 3 to 4 weeks old were split into four treatment groups: control; intranasally infected with Type 2 PRRSV NPB strain; intranasally infected with B/Brisbane/60/2008 virus; or intranasally coinfected with both viruses. Three pigs from each of the four treatment groups were necropsied 3 days post-infection(dpi) and thymus samples were collected for transcriptomic analysis. Differentially expressed gene (DEG) analysis was carried out using DeSeq2 based on the model treatment + E and g:Profiler was used to identify over enriched gene ontology (GO) terms and pathways. 205 genes were uniquely differentially expressed in the coinfected animals (not expressed in either single infection). 174 of these genes were downregulated and significantly over enriched for 121 GO terms and 17 pathways, including interferon signaling and antiviral mechanism by IFN stimulated genes. PRRSV has previously been reported to disrupt interferon signaling, which also inhibits influenza virus replication. These results may explain why influenzas are a common secondary infection to PRRSV.