Location: Virus and Prion ResearchTitle: Analysis of the swine tracheobronchial lymphnode transcriptomic response to infection with a Chinese highly pathogenic strain of porcine reproductive and respiratory syndrome virus) Author
|Kehrli jr, Marcus|
Submitted to: Genome Technology
Publication Type: Abstract only
Publication Acceptance Date: 8/15/2012
Publication Date: N/A
Citation: Interpretive Summary:
Technical 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) 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.