Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen of swine worldwide and causes considerable economic loss. Identifying specific cell signaling or activation pathways that associate with variation in PRRSV replication and macrophage function may lead to identification of novel gene targets for the control of PRRSV infection. Serial Analysis of Gene Expression (SAGE) was used to create and survey the transcriptome of in vitro mock-infected and PRRSV strain VR-2332-infected porcine alveolar macrophages (PAM) at 0, 6, 12, 16, and 24 hours after infection. The transcriptome data indicated changes in transcript abundance occurring in PRRSV-infected PAMs over time after infection with more than 590 unique tags with significantly altered transcript abundance levels identified (P < .01). Strikingly, innate immune genes (whose transcript abundances are typically altered in response to other pathogens or insults including IL-8, CCL4, and IL-1β) showed no or very little change at any time point following infection.
Highlights
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), the causative agent of porcine reproductive and respiratory syndrome (PRRS) in swine, is a member of the Arteriviridae family in the order Nidovirales
Examination of the Serial Analysis of Gene Expression (SAGE) data indicated that there were major changes in transcript abundance occurring in the PRRSV-infected porcine alveolar macrophage (PAM) based on more than 590 unique tags with significantly altered transcript abundance (P < .001 with Bonferroni correction)
The wealth of information obtained allows detection of altered transcription of genes involved in normal porcine alveolar macrophage physiology, as well as genes whose transcript abundance is altered by PRRSV infection
Summary
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), the causative agent of porcine reproductive and respiratory syndrome (PRRS) in swine, is a member of the Arteriviridae family in the order Nidovirales. PRRSV causes significant 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]. Clinical disease caused by PRRSV is highly variable, ranging from mild, subclinical infections to acute deaths of swine of any age [8]. Little is known about the interactions of PRRSV and host cells. PRRSV has been shown to replicate to varying degrees in peritoneal macrophages, pulmonary intravascular macrophages, type II pneumocytes, testicular germ cells, and PAMs [19,20,21,22]. The CD163 protein, sialoadhesin, and heparan sulphate have been reported to play significant role in helping PRRSV attach and be internalized into cells [23]
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