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Wild-type and innate immune-deficient mice are not susceptible to the Middle East respiratory syndrome coronavirus

机译:野生型和先天性免疫缺陷小鼠不易患中东呼吸综合征冠状病毒

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摘要

The Middle East respiratory syndrome coronavirus (MERS-CoV) is a newly emerging highly pathogenic virus causing almost 50 % lethality in infected individuals. The development of a small-animal model is critical for the understanding of this virus and to aid in development of countermeasures against MERS-CoV. We found that BALB/c, 129/SvEv and 129/SvEv STAT1 knockout mice are not permissive to MERS-CoV infection. The lack of infection may be due to the low level of mRNA and protein for the MERS-CoV receptor, dipeptidyl peptidase 4 (DPP4), in the lungs of mice. The low level of DPP4 in the lungs likely contributes to the lack of viral replication in these mouse models and suggests that a transgenic mouse model expressing DPP4 to higher levels is necessary to create a mouse model for MERS-CoV.
机译:中东呼吸综合症冠状病毒(MERS-CoV)是一种新兴的高致病性病毒,在感染的个体中造成近50%的致死率。小动物模型的发展对于理解这种病毒并帮助开发针对MERS-CoV的对策至关重要。我们发现,BALB / c,129 / SvEv和129 / SvEv STAT1基因敲除小鼠不允许MERS-CoV感染。缺乏感染可能是由于小鼠肺部MERS-CoV受体二肽基肽酶4(DPP4)的mRNA和蛋白水平较低。肺中低水平的DPP4可能导致这些小鼠模型中病毒复制的缺乏,这表明表达DPP4更高水平的转基因小鼠模型对于创建MERS-CoV的小鼠模型是必需的。

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