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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #280909
Title: Analysis of the swine tracheobronchial lymphnode transcriptomic response to infection with a Chinese highly pathogenic strain of porcine reproductive and respiratory syndrome virus

Author
item Miller, Laura
item FLEMING, DAMARIUS - Iowa State University
item ARBOGAST, ANDREW - Iowa State University
item Bayles, Darrell
item GUO, BAOQING - Iowa State University
item Lager, Kelly
item Henningson, Jamie
item Schlink, Sarah
item YANG, HAN-CHUN - China Agricultural University
item Faaberg, Kay
item Kehrli Jr, Marcus

Submitted to: BioMed Central (BMC) Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/31/2012
Publication Date: 10/30/2012
Citation: Miller, L.C., Fleming, D., Arbogast, A., Bayles, D.O., Guo, B., Lager, K.M., Henningson, J.N., Schlink, S.N., Yang, H.-C., Faaberg, K.S., Kehrli, Jr., M.E. 2012. Analysis of the swine tracheobronchial lymph node transcriptomic response to infection with a Chinese highly pathogenic strain of porcine reproductive and respiratory syndrome virus. BioMed Central (BMC) Veterinary Research. 8(1):208. Available: http://www.biomedcentral.com/1746-6148/8/208.

Interpretive Summary: The pig respiratory virus, porcine reproductive and respiratory syndrome virus (PRRSV), causes highly significant losses to the swine industry worldwide. The ability of the virus to persist in its host shows that it has mechanisms to evade host immune responses. This study examined the effect of a novel highly virulent porcine reproductive and respiratory virus (HP-PRRSV) on how genes are expressed in porcine tracheobronchial lymph nodes (TBLN) of United States swine. RNAseq analysis of gene expression was used because it allowed us to look at all genes expressed in these cells. We determined the normal levels of gene expression in normal, non-infected TBLN and then compared this to gene expression levels in US prototype PRRSV-infected pigs and HP-PRRSV-infected pigs at 14 days after infection. It is well established that many pathogens interfere with expression of specific genes that act to protect the host and clear the infection. There are specific cellular proteins that control expression of protective genes and future studies will look at how this virus may be inhibiting their function. This may possibly lead to a means for developing a vaccine that may act to limit or end an active PRRSV infection by restoring the cell's natural protective mechanisms.

Technical Abstract: Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen of swine worldwide. Emergence in 2006 of a novel highly pathogenic PRRSV (HP-PRRSV) isolate in China necessitated a comparative investigation into the host transcriptome response in tracheobronchial lymph nodes (TBLN) 14 days post-infection with HP-PRRSV rJXwn06, strain VR-2332 or sham inocula. RNA from each was prepared for next-generation sequencing. Amplified library constructs were directly sequenced and a list of sequence transcripts and counts was generated using an RNAseq analysis pipeline to determine differential gene expression. Transcripts were annotated and relative abundance was calculated based upon the number of times a given transcript was represented in the library. Results Major changes in transcript abundance occurred in response to infection with both PRRSV strains, each with over 630 differentially expressed transcripts. The largest increase in transcript level for either virus versus sham-inoculated controls were three serum amyloid A2 acute-phase isoforms. However, the degree of up or down-regulation of transcripts following infection with HP-PRRSV rJXwn06 was greater than transcript changes observed with US PRRSV VR-2332. Also, of 632 significantly altered transcripts within the HP-PRRSV rJXwn06 library 55 were upregulated and 69 were downregulated more than 3 fold, whilst in the US PRRSV VR2332 library only 4 transcripts were upregulated and 116 were downregulated more than 3 fold. Conclusions The magnitude of differentially expressed gene profiles detected in HP-PRRSV rJXwn06 infected pigs as compared to VR-2332 infected pigs was consistent with the increased pathogenicity of the HP-PRRSV in vivo.