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Mice transgenic for human angiotensin-converting enzyme 2 provide a model for SARS coronavirus infection

机译：为人类血管紧张素转化酶2转基因的小鼠提供了SARS冠状病毒感染的模型

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摘要

To establish a small animal model of severe acute respiratory syndrome (SARS), we developed a mouse model of human severe acute respiratory syndrome coronavirus (SARS-CoV) infection by introducing the human gene for angiotensin-converting enzyme 2 (hACE2) (the cellular receptor of SARS-CoV), driven by the mouse ACE2 promoter, into the mouse genome. The hACE2 gene was expressed in lung, heart, kidney, and intestine. We also evaluated the responses of wild-type and transgenic mice to SARS-CoV inoculation. At days 3 and 7 postinoculation, SARS-CoV replicated more efficiently in the lungs of transgenic mice than in those of wild-type mice. In addition, transgenic mice had more severe pulmonary lesions, including interstitial hyperemia and hemorrhage, monocytic and lymphocytic infiltration, protein exudation, and alveolar epithelial cell proliferation and desquamation. Other pathologic changes, including vasculitis, degeneration, and necrosis, were found in the extrapulmonary organs of transgenic mice, and viral antigen was found in brain. Therefore, transgenic mice were more susceptible to SARS-CoV than were wild-type mice, and susceptibility was associated with severe pathologic changes that resembled human SARS infection. These mice will be valuable for testing potential vaccine and antiviral drug therapies and for furthering our understanding of SARS pathogenesis.
机译：要建立严重急性呼吸综合征（SARS）的小动物模型，我们通过引入血管紧张素转化酶2（hACE2）的人类基因（细胞，将其开发为人类严重急性呼吸综合征冠状病毒（SARS-CoV）感染的小鼠模型小鼠ACE2启动子驱动的SARS-CoV受体）进入小鼠基因组。 hACE2基因在肺，心脏，肾脏和肠中表达。我们还评估了野生型和转基因小鼠对SARS-CoV接种的反应。接种后第3天和第7天，SARS-CoV在转基因小鼠肺部的复制比野生型小鼠更为有效。此外，转基因小鼠的肺部病变更为严重，包括间质充血和出血，单核细胞和淋巴细胞浸润，蛋白质渗出以及肺泡上皮细胞增殖和脱皮。在转基因小鼠的肺外器官中发现了其他病理变化，包括血管炎，变性和坏死，并且在脑中发现了病毒抗原。因此，转基因小鼠比野生型小鼠更容易感染SARS-CoV，而且易感性与严重的病理变化相关，类似于人的SARS感染。这些小鼠对于测试潜在的疫苗和抗病毒药物疗法以及进一步加深我们对SARS发病机理的了解将是有价值的。

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