畜牧兽医学报 ›› 2016, Vol. 47 ›› Issue (5): 962-969.doi: 10.11843/j.issn.0366-6964.2016.05.013

• 预防兽医 • 上一篇    下一篇

H5N1亚型禽流感病毒感染番鸭引起肺损伤和脑损伤的机制探索

李奇1,2,3#,叶昱5#,佟铁铸6#,刘洁1,2,3,刘杨1,2,4,章震1,2,4,苗配思1,2,4,高应棋1,2,4,张娇1,2,4,樊惠英1,2,3,4*,廖明1,2,3,4*   

  1. (1.华南农业大学 兽医学院,广州 510642;2.人兽共患病防控制剂国家地方联合工程实验室,广州 510642;3.农业部兽用疫苗创制重点实验室,广州 510642;4.广东省动物源性人兽共患病预防与控制重点实验室,广州 510642;5.江西农业大学 动物科技学院,南昌 330045;6.惠州出入境检验检疫局,惠州 516006)
  • 收稿日期:2015-10-22 出版日期:2016-05-23 发布日期:2016-05-23
  • 通讯作者: 廖明,男,教授,E-mail:mliao@scau.edu.cn;樊惠英,教授,E-mail:fanhy@scau.edu.cn
  • 作者简介:李奇(1991-),男,河南长垣人,硕士生,主要从事动物传染病的研究,E-mail: liqi19910705@126.com;叶昱(1986-),男,湖南长沙人,助理研究员,主要从事动物传染病的研究,E-mail:yy6157832@163.com;佟铁铸(1979-),男,辽宁沈阳人,兽医师,硕士;#对本文贡献相同,同为第一作者
  • 基金资助:

    广东省自然科学基金(2014A030313462);广东省H7N9禽流感科技发展专项(20140224);H7N9联合研究专项[(2014) No.1046]

The Mechanism of Lung Injury and Brain Injury in Muscovy Ducks Infected with H5N1 Avian Influenza Virus

LI Qi1,2,3# ,YE Yu5# ,TONG Tie-zhu6# ,LIU Jie1,2,3,LIU Yang1,2,4,ZHANG Zhen1,2,4,MIAO Pei-si1,2,4,GAO Ying-qi1,2,4,ZHANG Jiao1,2,4,FAN Hui-ying1,2,3,4* ,LIAO Ming1,2,3,4*   

  1. (1.College of Veterinary Medicine,South China Agricultural University,Guangzhou 510642,China;
    2.National and Regional Joint Engineering Laboratory for Medicament of Zoonosis Prevention and Control,Guangzhou 510642,China;3.Key Laboratory of Animal Vaccine Development,Ministry of Agriculture,Guangzhou 510642,China;4.Key Laboratory of Zoonosis Prevention and Control of Guangdong Province,Guangzhou 510642,China;5.College of Animal Science and Technology,Jiangxi Agricultural University,Nanchang 330045,China;6.Huizhou Entry-Exit Inspection and Quarantine Bureau,Huizhou 516006,China)
  • Received:2015-10-22 Online:2016-05-23 Published:2016-05-23

摘要:

旨在初步探讨H5N1禽流感病毒引起番鸭肺和脑组织损伤的潜在机制。采用两株H5N1禽流感病毒DK383 (A/Duck/Guangdong/383/2008) 和DK212 (A/Duck/Guangdong/212/2004)分别感染番鸭,于感染后1、2和3 d取肺、脑组织,进行病理学观察,并检测病毒复制水平及损伤相关因子的变化情况。结果表明,DK383株感染番鸭后,引起明显的呼吸困难和神经症状,致死率为70%,DK212株则无明显临床症状。病理组织学变化显示,DK383感染番鸭后造成了肺损伤和脑损伤,大脑组织神经元发生广泛性变性、坏死,肺淤血出血严重;而DK212组和空白组未见明显病理变化。与DK212株相比,DK383株在肺和脑组织内的病毒复制水平更高,激活TLR-TRIF-TRAF6通路的能力更强,诱导了更强的免疫反应。本研究提示,DK383在番鸭肺和脑组织高水平复制,引起番鸭产生过度的先天免疫应答反应,从而造成肺和脑组织损伤。

Abstract:

This experiment was conducted to preliminarily investigate the mechanisms of lung injury and brain injury in duck infected with avian influenza virus.Ducks were intranasally infected with DK383 virus (A/Duck/Guangdong/383/2008) and DK212 virus (A/Duck/Guangdong/212/2004),respectively.The lung and brain were collected at 1,2,and 3 days post infection (dpi) for pathological observation,RNA extraction and detection of the proliferation of virus.The expression of several genes mRNA were detected by RT-PCR.DK383 was highly pathogenic with high mortality rate of 70% and severe neurological sign.The histopathological observation of duck infected with DK383 showed extensive neuronal degeneration and necrosis occurred in the brain tissue,severe acute congestion and hemorrhage in the lung.Compared to DK212,DK383 replicated more efficiently in the lung and brain and activated TLR-TRIF-TRAF6 signaling more strikingly.The improper regulation of DK383-induced immune response and the viral replication competent are correlated with the severity of the disease.

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