Aberrant host immune response induced by highly virulent PRRSV identified by digital gene expression tag profiling

Shuqi Xiao,Yaosheng Chen,Yuna Niu,Limei Qin,Xiaohong Liu,Jianyu Jia,Delin Mo,Xiao Zhao,Xiangchun Yu,Qiwei Wang

doi:10.1186/1471-2164-11-544

Shuqi Xiao, Yaosheng Chen + Show 8 more

Open Access

https://doi.org/10.1186/1471-2164-11-544

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Journal: BMC Genomics	Publication Date: Oct 7, 2010
Citations: 120	License type: CC BY 4.0

Affiliation: Sun Yat-sen University

Abstract

BackgroundThere was a large scale outbreak of the highly pathogenic porcine reproductive and respiratory syndrome (PRRS) in China and Vietnam during 2006 and 2007 that resulted in unusually high morbidity and mortality among pigs of all ages. The mechanisms underlying the molecular pathogenesis of the highly virulent PRRS virus (H-PRRSV) remains unknown. Therefore, the relationship between pulmonary gene expression profiles after H-PRRSV infection and infection pathology were analyzed in this study using high-throughput deep sequencing and histopathology.ResultsH-PRRSV infection resulted in severe lung pathology. The results indicate that aberrant host innate immune responses to H-PRRSV and induction of an anti-apoptotic state could be responsible for the aggressive replication and dissemination of H-PRRSV. Prolific rapid replication of H-PRRSV could have triggered aberrant sustained expression of pro-inflammatory cytokines and chemokines leading to a markedly robust inflammatory response compounded by significant cell death and increased oxidative damage. The end result was severe tissue damage and high pathogenicity.ConclusionsThe systems analysis utilized in this study provides a comprehensive basis for better understanding the pathogenesis of H-PRRSV. Furthermore, it allows the genetic components involved in H-PRRSV resistance/susceptibility in swine populations to be identified.

Highlights

There was a large scale outbreak of the highly pathogenic porcine reproductive and respiratory syndrome (PRRS) in China and Vietnam during 2006 and 2007 that resulted in unusually high morbidity and mortality among pigs of all ages
IRF3 plays an important role in typeI IFN gene expression and the present study demonstrated that IRF3 gene expression was suppressed during highly virulent PRRS virus (H-PRRSV) infection (Figure 5D)
From the data presented a model summarizing the relationship between pulmonary gene expression profiles and infection pathology has been proposed (Figure 8)

Summary

Introduction

There was a large scale outbreak of the highly pathogenic porcine reproductive and respiratory syndrome (PRRS) in China and Vietnam during 2006 and 2007 that resulted in unusually high morbidity and mortality among pigs of all ages. A further study concerning the effect of the VR-2332 PRRSV strain (NA PRRSV) on PAM function utilized serial analysis of gene expression and demonstrated that expression of MX1 and USP were significantly up-regulated 24 hours postinfection (h pi) [9]. These studies have provided a genome-wide gene expression profile of PAMs in vitro following infection with EU PRRSV or NA PRRSV. PRRSV infection causes widespread apoptosis in pulmonary and lymphoid tissues of infected pigs [10], but the cause of the increased severity of the symptoms and the unusually high mortality of pigs infected with H-PRRSV (a mutant North American highly virulent porcine reproductive and respiratory syndrome virus) remains unknown

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