Comparative analysis of apoptotic changes in peripheral immune organs and lungs following experimental infection of piglets with highly pathogenic and classical porcine reproductive and respiratory syndrome virus

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• 作者：Gang Wang (1)
  Yuli He (1)
  Yabin Tu (1)
  Yonggang Liu (1)
  En-Min Zhou (2)
  Zifeng Han (1) (3)
  Chenggang Jiang (1)
  Shujie Wang (1)
  Wenda Shi (1)
  Xuehui Cai (1)
  
• 关键词：Highly pathogenic PRRSV ; Classical PRRSV ; Peripheral immune organs ; Lung ; Cell apoptosis
• 刊名：Virology Journal
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：11
• 期：1
• 全文大小：459 KB
• 作者单位：Gang Wang (1)
  Yuli He (1)
  Yabin Tu (1)
  Yonggang Liu (1)
  En-Min Zhou (2)
  Zifeng Han (1) (3)
  Chenggang Jiang (1)
  Shujie Wang (1)
  Wenda Shi (1)
  Xuehui Cai (1)
  
  1. State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang Province, 150001, PR China
  2. Department of Preventive Veterinary Medicine, College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, 712100, PR China
  3. Northeast Agricultural University, Harbin, 150030, PR China
  
• ISSN：1743-422X

文摘

Background Our previous studies have demonstrated that piglets infected with highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) may develop significant thymus atrophy, which related to thymocytes apoptosis. However, apart from that detected in the thymus, there are no reports describing cell apoptosis induced by HP-PRRSV infection. In this study, we analyzed comparatively the pathological changes, cell apoptosis and viral load in peripheral immune organs including tonsil, inguinal lymph nodes (ILNs) and spleen and lungs following experimental infection of piglets with HP-PRRSV HuN4 and classical PRRSV CH-1a. Findings HP-PRRSV HuN4 exhibited much stronger cell tropism than CH-1a in immune organs and lungs of piglets. HuN4 infection led to the serious injuries in tonsils, ILNs, spleens and lungs, especially apoptosis in these organs was significant. Conclusions HuN4 infection induced severe lesions (gross pathology, histopathology and cell apoptosis) in the peripheral immune organs and lungs of infected piglets. Large numbers of apoptotic cells in immune organs and lung induced by HuN4 may play a role in the pathogenesis of the HP-PRRS and the distinct injuries caused by HuN4 infection may be associated with the high mortality rate of HP-PRRS in pigs.