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

• Published in: BMC genomics 2010-10, Vol.11 (1), p.544-544, Article 544
• Main Authors: Xiao, Shuqi, Mo, Delin, Wang, Qiwei, Jia, Jianyu, Qin, Limei, Yu, Xiangchun, Niu, Yuna, Zhao, Xiao, Liu, Xiaohong, Chen, Yaosheng
• Format: Article
• Language: English
• Subjects: Adaptive Immunity - genetics; Animals; Apoptosis; Bioinformatics; Causes of; Cell Death; Cluster Analysis; Cytokines - blood; DNA sequencing; Fever; Gene expression; Gene Expression Profiling - methods; Gene Library; Genes; Genetic aspects; Genetic research; Genomes; Genomics; Health aspects; Host-Pathogen Interactions - genetics; Host-Pathogen Interactions - immunology; Immune response; Immunity - genetics; Immunity, Innate - genetics; Infection; Life sciences; Lung - immunology; Lung - metabolism; Lung - pathology; Lung - virology; Medical research; Medicine, Experimental; Models, Genetic; Nucleotide sequencing; Pathogenesis; Physiological aspects; Polymerase Chain Reaction; Porcine reproductive and respiratory syndrome; Porcine Reproductive and Respiratory Syndrome - blood; Porcine Reproductive and Respiratory Syndrome - genetics; Porcine Reproductive and Respiratory Syndrome - pathology; Porcine Reproductive and Respiratory Syndrome - virology; Porcine respiratory and reproductive syndrome virus - pathogenicity; Proteins; Reproducibility of Results; Rodents; Signal Transduction - genetics; Studies; Sus scrofa - genetics; Sus scrofa - virology; Swine - genetics; Swine - immunology; Swine - virology; Virulence; Virulence (Microbiology)
• ISSN: 1471-2164; 1471-2164
• DOI: 10.1186/1471-2164-11-544

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. 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. H-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. The 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.