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新分离呼肠病毒BYD1株实验感染食蟹猴的病理学改变及发病机制
引用本文:何诚,朱虹,何君,左庭婷,雷鸣,檀华,甘永华,黄如统,端青. 新分离呼肠病毒BYD1株实验感染食蟹猴的病理学改变及发病机制[J]. 军事医学科学院院刊, 2003, 27(6): 404-405,440
作者姓名:何诚  朱虹  何君  左庭婷  雷鸣  檀华  甘永华  黄如统  端青
作者单位:1. 中国农业大学实验动物研究所,北京,100094
2. 军事医学科学院微生物流行病研究所,北京,100071
摘    要:目的:系统观察新分离呼肠病毒感染食蟹猴的病理学变化,探讨其发病机制。方法:用从SARS患者分离的呼肠病毒BYD1株通过滴鼻和静脉注射两种途径,感染4只食蟹猴(每组2只)。每组分别在感染后7d和33d各处死1只,进行肺脏、心肌、肝脏、脾脏、肾脏、肠、脑和淋巴等组织病理学检查。结果:肉眼观察感染猴肺组织可见水肿和红白相间的实变。病理组织学变化主要集中在肺脏、脾脏、淋巴结和全身小静脉。肺脏表现局部肺泡腔出血,并有蛋白液渗出。肺泡间隔充血、淤血、水肿,导致肺泡壁增厚。支气管上皮细胞和黏膜纤毛脱落,支气管周围单核细胞浸润。脾脏、淋巴结白髓减少,红髓淤血,发生中心淋巴细胞数量减少。全身组织器官小静脉明显淤血。结论:食蟹猴实验感染呼肠病毒BYD1株后,出现间质性肺炎,脾脏、淋巴结萎缩和全身小静脉淤血等一系列组织病理学特征。病毒感染后,受侵害肺脏出现血氧交换障碍和免疫器官功能下降是导致食蟹猴发病的内在机制。新分离的呼肠病毒感染食蟹猴出现的病理学变化提示可以作为严重呼吸综合征的病理学模型。

关 键 词:呼肠病毒(BYD1株) 食蟹猴 病理学 发病机制
文章编号:1000-5501(2003)06-0404-03

Pathological changes and pathogenesis of experimental infection of cynomolgus monkeys with reovirus strain BYD1
HE Cheng ,ZHU Hong ,HE Jun ,ZUO Ting-Ting ,LEI Ming ,TAN Hua ,GAN Yong-Hua ,HUANG Ru-Tong ,DUAN Qing. Pathological changes and pathogenesis of experimental infection of cynomolgus monkeys with reovirus strain BYD1[J]. Bulletin of the Academy of Military Medical Sciences, 2003, 27(6): 404-405,440
Authors:HE Cheng   ZHU Hong   HE Jun   ZUO Ting-Ting   LEI Ming   TAN Hua   GAN Yong-Hua   HUANG Ru-Tong   DUAN Qing
Affiliation:HE Cheng 1,ZHU Hong 2,HE Jun 2,ZUO Ting-Ting 2,LEI Ming 1,TAN Hua 2,GAN Yong-Hua 2,HUANG Ru-Tong 2,DUAN Qing 2*
Abstract:Objective:To observe the pathological change of experimental infection of cynomolgus monkeys (crab-eating monkeys) with reovirus (strain BYD1).Methods:Four cynomolgus monkeys were divided into two groups. Two were inoculated intravenously and others were inoculated by dropping into the nose with reovirus (strain BYD1) isolated recently from one SARS patient.One monkey from each group was sacrificed on day 7 and day 33,respectively. The histopathological changes in monkeys' lung,heart,liver,spleen, kidney, brain and intestine were examined under microscope.Results:The lung of infected monkey showed edema and red-white consolidation on gross examination. The histopathological changes focused on lung, spleen, lymph and small vein of many organs. The predominant exudative inflammation and hemorrhagic pneumonia were observed evidently associated with monocyte proliferation, congestion and permeation of pulmonary capillaries and thickening of interalveolar septa. The lymphocyte decreased in cortex of lymph node and white pulp of spleen. Stasis occurred in small vein and capillary of most of the tissues. No other pathologic change could be found both in heart and liver tissue. Conclusion:The reovirus (strain BYD1)could induce a series of clinical pathological syndrome in cynomolgus monkeys such as immunological responses and acute pulmonary interstitial exudative inflammation. The extra-pulmonary organs, such as lymph nodes and spleen, showed extensive extravasated inflammation. It is suggested that infection of cynomolgus monkeys by reovirus (strain BYD1) can be used as an animal model to study the pathology of SARS.
Keywords:reovirus(strain BYD1)  cynomolgus monkey  pathology  pathogenesis
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