understanding prrsv infection in porcine lung based on genome-wide transcriptome response identified by deep sequencing基于全基因组转录组理解prrsv感染猪肺反应被深度测序.pdfVIP

understanding prrsv infection in porcine lung based on genome-wide transcriptome response identified by deep sequencing基于全基因组转录组理解prrsv感染猪肺反应被深度测序.pdf

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understanding prrsv infection in porcine lung based on genome-wide transcriptome response identified by deep sequencing基于全基因组转录组理解prrsv感染猪肺反应被深度测序

Understanding PRRSV Infection in Porcine Lung Based on Genome-Wide Transcriptome Response Identified by Deep Sequencing Shuqi Xiao, Jianyu Jia, Delin Mo, Qiwei Wang, Limei Qin, Zuyong He, Xiao Zhao, Yuankai Huang, Anning Li, Jingwei Yu, Yuna Niu, Xiaohong Liu, Yaosheng Chen* State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China Abstract Porcine reproductive and respiratory syndrome (PRRS) has been one of the most economically important diseases affecting swine industry worldwide and causes great economic losses each year. PRRS virus (PRRSV) replicates mainly in porcine alveolar macrophages (PAMs) and dendritic cells (DCs) and develops persistent infections, antibody-dependent enhancement (ADE), interstitial pneumonia and immunosuppression. But the molecular mechanisms of PRRSV infection still are poorly understood. Here we report on the first genome-wide host transcriptional responses to classical North American type PRRSV (N-PRRSV) strain CH 1a infection using Solexa/Illumina’s digital gene expression (DGE) system, a tag- based high-throughput transcriptome sequencing method, and analyse systematically the relationship between pulmonary gene expression profiles after N-PRRSV infection and infection pathology. Our results suggest that N-PRRSV appeared to utilize multiple strategies for its replication and spread in infected pigs, including subverting host innate immune response, inducing an anti-apoptotic and anti-inflammatory state as well as developing ADE. Upregulation expression of virus-induced pro-inflammatory cytokines, chemokines, adhesion molecules and inflammatory enzymes and inflammatory cells, antibodies, complement activation were likely to result in the development of inflammatory

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