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作 者:李奇[1,2,3] 叶昱[4] 佟铁铸[5] 刘洁[1,2,3] 刘杨[1,2,6] 章震[1,2,6] 苗配思 高应棋 张娇[1,2,6] 樊惠英[1,2,3,6] 廖明[1,2,3,6]
机构地区:[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]江西农业大学动物科技学院,南昌330045 [5]惠州出入境检验检疫局,惠州516006 [6]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
出 处:《畜牧兽医学报》2016年第5期962-969,共8页ACTA VETERINARIA ET ZOOTECHNICA SINICA
基 金: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]
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3d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-TRIFTRAF6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。This experiment was conducted to preliminarily investigate the mechanisms of lung in- jury 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 expres- sion 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 in- fected with DK383 showed extensive neuronal degeneration and necrosis occurred in the brain tis- sue,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.
分 类 号:S858.325[农业科学—临床兽医学]
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