Department of Veterinary Pathology, Armed Forces Institutes of Pathology, Washington, District of Columbia, USA.
J Infect Dis. 2011 Nov;204 Suppl 3:S986-90. doi: 10.1093/infdis/jir335.
We evaluated the susceptibility to Ebola and Marburg virus infection of mice that cannot respond to interferon (IFN)-α/β and IFN-γ because of deletion of the STAT-1 gene. A mouse-adapted Zaire ebolavirus (ZEBOV) caused rapidly lethal disease; wild-type ZEBOV and Sudan Ebolavirus and 4 different Marburg virus strains produced severe, but more slowly progressive illness; and Reston Ebolavirus caused mild disease that was late in onset. The virulence of each agent was mirrored by the pace and severity of pathologic changes in the liver and lymphoid tissues. A virus-like particle vaccine elicited strong antibody responses but did not protect against mouse-adapted ZEBOV challenge.
我们评估了不能对干扰素（IFN）-α/β和 IFN-γ产生反应的 STAT-1 基因缺失小鼠对埃博拉和马尔堡病毒感染的易感性。一种适应于小鼠的扎伊尔埃博拉病毒（ZEBOV）引起了快速致命的疾病；野生型 ZEBOV 和苏丹埃博拉病毒以及 4 种不同的马尔堡病毒株引起了严重但进展更缓慢的疾病；而莱斯顿埃博拉病毒则引起了发病较晚的轻度疾病。每种病原体的毒力都反映在肝脏和淋巴组织病理变化的速度和严重程度上。一种类似病毒的颗粒疫苗引起了强烈的抗体反应，但不能预防适应于小鼠的 ZEBOV 挑战。
