Experimental infection of macaques with the human reovirus BYD1 strain: An animal model for the study of the severe acute respiratory syndrome
Experimental infection of macaques with the human reovirus BYD1 strain: An animal model for the study of the severe acute respiratory syndrome
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DOI：
10.1089/dna.2005.24.491
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发表时间：
2005-08-01
影响因子：
3.1
通讯作者：
Duan, Q
中科院分区：
文献类型：
--
作者：
He, C;Pang, WY;Duan, Q
进行了实验研究，以确定一个新分离的呼肠孤病毒（ReoV）从严重急性呼吸综合征（SARS）患者的病原学这种新描述的严重呼吸综合征的作用。用这种呼肠孤病毒（BYD 1）接种四只食蟹猴，试图复制SARS中观察到的感染和病理。每天三次监测受感染猴子的体温，并定期收集血液和粪便样品用于特异性免疫学测定。在接种后第7天和第33天，进行尸检以进行病理学评估和病原体分离。4只感染猕猴在接种后第3天和第4天出现发热，并持续发热4 - 6天。记录的动物最高温度为40.4摄氏度。经过一段恢复期后，猕猴又出现了第二次发热。通过静脉途径注射的呼肠孤病毒的抗体滴度高于鼻腔中的抗体滴度。四只猕猴表现出弥漫性肺泡损伤，其特征为出血性肺炎、血清血性渗出物、透明膜形成和II型肺细胞增生，与SARS患者中观察到的相似。淋巴结皮质和脾白色髓中的淋巴细胞减少。通过病毒分离和RT-PCR检测肺炎组织中的ReoV。感染了新分离的呼肠孤病毒的猕猴出现了与SARS患者相似的发热、弥漫性肺泡损伤和肺间质炎症。这些证据表明，ReoV可能在SARS的病因学中起主要作用。
Experimental studies were performed to determine the role of a newly isolated reovirus (ReoV) from a severe acute respiratory syndrome (SARS) patient in the etiology of this newly described serious respiratory syndrome. Four cynomologus macaques were inoculated with this reovirus (BYD1) in an attempt to replicate the infection and pathology observed in SARS. The body temperature of the infected monkeys was monitored three times a day, and blood and fecal samples were periodically collected for specific immunology determinations. On days 7 and 33 after inoculation, necropsies for pathological accessment and pathogen isolation were performed. The four infected macaques developed a fever on days 3 and 4 after inoculation, and maintainted a febrile state for 4 - 6 days. The highest temperature in the animals recorded was 40.4 degrees C. After a recovery phase, the macaques developed a second febrile condition. Antibody titers against the reovirus injected by the intravenous route occurred in higher number than those in the nasal cavity. Four macaque monkeys demonstrated diffuse alveolar damage, characterized by hemorrhagic pneumonia, serosanguineous exudates, formation of hyaline membranes, and type II pneumocyte hyperplasia, which were similar to those that have been noted in SARS patients. Lymphocytes decreased in the cortex of the lymph node and in the white pulp of the spleen. ReoV was detected in pneumonic tissue by virus isolation and RT-PCR. The macaques infected with the newly isolated reovirus developed a fever, diffuse alveolar damage and pulmonary interstitial inflammation similar to that noted in SARS patients. This evidence demonstrates that ReoV might have a primary role in the etiology of SARS.