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

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.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.Porcine reproductive and respiratory syndrome virus (PRRSV), the causative agent of PRRS in swine, is a member of the Arteriviridae family in the order Nidovirales. PRRSV causes highly significant economic losses to the swine industry worldwide [1] as a result of both reproductive failure (late-term abortions and stillbirths) in pregnant sows and respiratory disease (pneumonia) in nursery and grower/finishing pigs [2]. Infection with PRRSV also predisposes pigs to infection by bacterial pathogens as well as other viral pathogens [3-7], as such, PRRSV is a key etiological agent of the porcine respiratory disease complex (PRDC). Clinical disease caused by PRRSV is highly variable, ranging from mild, subclinical infection to acute death of adult animals [8]. Differences in virulence have been attributed to numerous factors including host genetics, management practices, and virus strain heterogeneity [9-16]. Relatively little is known about the interactions of PRRSV and host cells. The lymph node is an anatomic site where the innate immune respo