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Open Access Research article

Analysis of the swine tracheobronchial lymph node transcriptomic response to infection with a Chinese highly pathogenic strain of porcine reproductive and respiratory syndrome virus

Laura C Miller1*, Damarius Fleming2, Andrew Arbogast3, Darrell O Bayles4, Baoqing Guo5, Kelly M Lager1, Jamie N Henningson1, Sarah N Schlink1, Han-Chun Yang6, Kay S Faaberg1 and Marcus E Kehrli1

Author Affiliations

1 Virus and Prion Research Unit, National Animal Disease Center-USDA-ARS, Ames, Iowa, 50010, USA

2 Inter-departmental Genetics, Iowa State University, Ames, Iowa, 50011, USA

3 Department of Computer Science, Iowa State University, Ames, Iowa, 50011, USA

4 Infectious Bacterial Diseases Research Unit, National Animal Disease Center-USDA-ARS, Ames, Iowa, 50010, USA

5 Veterinary Diagnostic & Production Animal Medicine, Iowa State University, Ames, Iowa, 50011, USA

6 China Agricultural University, Beijing, China

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BMC Veterinary Research 2012, 8:208  doi:10.1186/1746-6148-8-208

Published: 30 October 2012

Abstract

Background

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) 13 days post-infection with HP-PRRSV rJXwn06, PRRSV 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 either PRRSV strain, 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 up-regulated and 69 were down-regulated more than 3-fold, whilst in the US PRRSV VR-2332 library only 4 transcripts were up-regulated and 116 were down-regulated 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.