The pathogenesis of Rift Valley fever virus in the mouse model
The pathogenesis of Rift Valley fever virus in the mouse model
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DOI：
10.1016/j.virol.2010.08.016
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发表时间：
2010-11-25
期刊：
影响因子：
3.7
通讯作者：
Hensley, Lisa E.
中科院分区：
文献类型：
--
作者：
Smith, Darci R.;Steele, Keith E.;Hensley, Lisa E.
目前还没有详细的研究描述裂谷热病毒在小鼠模型中的发病机制。需要一个充分表征的裂谷热小动物模型来评价潜在的疫苗和治疗方法。在这项研究中，我们的特点是RVFV的发病机制在整个疾病过程中的小鼠。感染产生高滴度病毒血症，并表现出RVFV对各种组织和单个细胞类型的嗜性。肝细胞的压倒性感染，伴随着细胞凋亡，是感染的主要后果。大多数小鼠在感染重度肝炎后3 - 6天死亡或被安乐死。剩下的小鼠有效地清除了肝脏和血液中的病毒，但表现出神经侵袭并发展为全脑炎。此外，我们的特点是一些其他的病毒学，临床病理学和组织病理学特征的RVFV感染小鼠。因此，小鼠模型模拟了急性肝炎和迟发性脑炎，而这两种疾病是严重人类裂谷热的主要特征。爱思唯尔公司出版
Detailed studies describing the pathogenesis of Rift Valley fever (RVF) virus (RVFV) in the mouse model are lacking. A fully characterized small animal model of RVF is needed to evaluate potential vaccines and therapeutics. In this study, we characterized the pathogenesis of RVFV throughout the disease course in mice. Infection produced high-titer viremia and demonstrated RVFV tropism for a variety of tissue and individual cell types. Overwhelming infection of hepatocytes, accompanied by apoptosis, was a major consequence of infection. The majority of mice died or were euthanatized between days 3 and 6 postinfection with severe hepatitis. The remaining mice effectively cleared virus from the liver and blood, but exhibited neuroinvasion and developed panencephalitis. In addition, we characterized a number of other virological, clinicopathological, and histopathological features of RVFV infection in mice. The mouse model therefore mimics both the acute-onset hepatitis and delayed-onset encephalitis that are dominant features of severe human RVF. Published by Elsevier Inc.