Comparison of the Pathogenicity of Nipah Virus Isolates from Bangladesh and Malaysia in the Syrian Hamster

Comparison of the Pathogenicity of Nipah Virus Isolates from Bangladesh and Malaysia in the Syrian Hamster
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DOI:
10.1371/journal.pntd.0002024
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发表时间:
2013-01-01
影响因子:
3.8
通讯作者:
Prescott, Joseph
Prescott, Joseph
中科院分区:
医学2区
文献类型:
--
作者:
DeBuysscher, Blair L.;de Wit, Emmie;Prescott, Joseph

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尼帕病毒是一种人畜共患病原体,可导致人类严重疾病。发病机制尚未得到很好的描述。第一次尼帕病毒爆发发生在马来西亚,那里的人类疾病有很强的神经系统成分。随后在孟加拉国和印度发生了疫情,这些疫情的传播和疾病过程似乎与马来西亚疫情不同。在此之前,几乎所有的尼帕病毒体外和体内研究,包括疫苗和发病机制研究,都使用了来自最初马来西亚爆发的病毒分离株(NiV-M)。为了研究NiV-M和来自孟加拉国的尼帕病毒分离株(NiV-B)之间的潜在差异,我们比较了NiV-M和NiV-B的体外和体内感染。在仓鼠肾细胞中,NiV-M感染导致广泛的合胞体形成和细胞病变效应,而NiV-B感染导致很少或没有形态学变化。在体内,NiV-M感染的叙利亚仓鼠加速病毒复制,病理和死亡时相比,NiV-B感染的动物。NiV-M感染也导致宿主免疫应答基因在较早的时间点激活。致病性不仅是病毒复制直接作用的结果,而且可能还具有免疫致病成分。在仓鼠中观察到的NiV-M和NiV-B病原体之间的差异可能与在人类病例中观察到的差异有关。NiV-B感染的仓鼠模型的表征允许进一步研究导致最近人类爆发的尼帕病毒株。该模型可用于研究NiV-B的发病机制,传播和可用于控制暴发的对策。
Nipah virus is a zoonotic pathogen that causes severe disease in humans. The mechanisms of pathogenesis are not well described. The first Nipah virus outbreak occurred in Malaysia, where human disease had a strong neurological component. Subsequent outbreaks have occurred in Bangladesh and India and transmission and disease processes in these outbreaks appear to be different from those of the Malaysian outbreak. Until this point, virtually all Nipah virus studies in vitro and in vivo, including vaccine and pathogenesis studies, have utilized a virus isolate from the original Malaysian outbreak (NiV-M). To investigate potential differences between NiV-M and a Nipah virus isolate from Bangladesh (NiV-B), we compared NiV-M and NiV-B infection in vitro and in vivo. In hamster kidney cells, NiV-M-infection resulted in extensive syncytia formation and cytopathic effects, whereas NiV-B-infection resulted in little to no morphological changes. In vivo, NiV-M-infected Syrian hamsters had accelerated virus replication, pathology and death when compared to NiV-B-infected animals. NiV-M infection also resulted in the activation of host immune response genes at an earlier time point. Pathogenicity was not only a result of direct effects of virus replication, but likely also had an immunopathogenic component. The differences observed between NiV-M and NiV-B pathogeneis in hamsters may relate to differences observed in human cases. Characterization of the hamster model for NiV-B infection allows for further research of the strain of Nipah virus responsible for the more recent outbreaks in humans. This model can be used to study NiV-B pathogenesis, transmission, and countermeasures that could be used to control outbreaks.