Sanchez-Lanier M, Davis L E, Blisard K S, Woodfin B M, Wallace J M, Caskey L S
Neurology Service, Veterans Administration Medical Center, Albuquerque, New Mexico.
Int J Exp Pathol. 1991 Oct;72(5):489-500.
To develop an animal model of Reye's syndrome using a virus associated with the human disease, mice were intravenously inoculated with influenza A/PR8 virus (LD50 4000 haemagglutinin units). One to 3 days later the mice developed lethargy, seizures, coma and death. The cerebrospinal fluid cell count was normal. Serum aspartate aminotransferase levels increased 24-fold. Diffuse microvesicular fatty metamorphosis along with multiple small foci of necrosis developed in the liver. Influenza virus-like particles were seen by electron microscopy in the liver, primarily in areas of liver necrosis, but were not seen in the brain. Cerebral oedema without inflammation developed in the brain. Limited viral replication occurred within the liver. Influenza viral antigens were seen in 5-20% of hepatocytes from both necrotic and non-necrotic areas as well as in brain endothelial cells. Many of the clinical, biochemical and pathologic features of the mouse illness resemble those seen in Reye's syndrome. However, this model differs from the human disease in that focal areas of liver necrosis occurred along with limited complete viral replication in liver.
为了使用与人类疾病相关的病毒建立瑞氏综合征的动物模型,将甲型流感病毒A/PR8(半数致死量为4000血凝素单位)静脉接种到小鼠体内。1至3天后,小鼠出现嗜睡、惊厥、昏迷和死亡。脑脊液细胞计数正常。血清天冬氨酸转氨酶水平升高了24倍。肝脏出现弥漫性微泡性脂肪变性以及多个小坏死灶。通过电子显微镜在肝脏中观察到流感病毒样颗粒,主要在肝坏死区域,但在脑中未观察到。脑中出现无炎症的脑水肿。肝脏内发生有限的病毒复制。在坏死和非坏死区域的5%至20%的肝细胞以及脑内皮细胞中可见流感病毒抗原。小鼠疾病的许多临床、生化和病理特征与瑞氏综合征中所见的相似。然而,该模型与人类疾病的不同之处在于,肝坏死灶与肝脏中有限的完全病毒复制同时出现。