A new model for Hendra virus encephalitis in the mouse.
A new model for Hendra virus encephalitis in the mouse.
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DOI：
10.1371/journal.pone.0040308
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Wang LF
中科院分区：
文献类型：
--
作者：
Dups J;Middleton D;Yamada M;Monaghan P;Long F;Robinson R;Marsh GA;Wang LF
亨德拉病毒（HeV）感染人类的特征是流感样疾病，其可进展为肺炎或脑炎并导致死亡。HeV感染的发病机制知之甚少，缺乏小鼠模型限制了发病机制研究的机会。在这个项目中，我们重新评估了小鼠作为HeV感染的动物模型的作用，发现小鼠在鼻内暴露后对HeV感染易感，老年小鼠可靠地发展为脑炎疾病。我们提出了一个顺行的神经侵入脑的路线，可能是沿着嗅神经。这一点得到了以下证据的支持：在没有病毒血症的情况下发生脑炎，以及鼻内攻击动物脑中病毒抗原沿着嗅觉通路的顺序分布。在我们的研究中，小鼠发生了短暂的下呼吸道感染，而没有进展为其他动物模型常见的病毒血症和全身性血管炎。这些研究报告了一种新的HeV脑炎动物模型，这将允许更详细地研究HeV感染的神经发病机制，特别是中枢神经系统内的病毒传播模式和可能的隔离;调查调节病毒血症和全身性疾病发展的机制;并为人类患者提供改进的治疗方案。
Hendra virus (HeV) infection in humans is characterized by an influenza like illness, which may progress to pneumonia or encephalitis and lead to death. The pathogenesis of HeV infection is poorly understood, and the lack of a mouse model has limited the opportunities for pathogenetic research. In this project we reassessed the role of mice as an animal model for HeV infection and found that mice are susceptible to HeV infection after intranasal exposure, with aged mice reliably developing encephalitic disease. We propose an anterograde route of neuroinvasion to the brain, possibly along olfactory nerves. This is supported by evidence for the development of encephalitis in the absence of viremia and the sequential distribution of viral antigen along pathways of olfaction in the brain of intranasally challenged animals. In our studies mice developed transient lower respiratory tract infection without progressing to viremia and systemic vasculitis that is common to other animal models. These studies report a new animal model of HeV encephalitis that will allow more detailed studies of the neuropathogenesis of HeV infection, particularly the mode of viral spread and possible sequestration within the central nervous system; investigation of mechanisms that moderate the development of viremia and systemic disease; and inform the development of improved treatment options for human patients.
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影响因子：
0.8
作者：
Middleton, DJ;Westbury, HA;Hyatt, AD
通讯作者：
Hyatt, AD
影响因子：
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作者：
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作者：
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