| Literature DB >> 32380511 |
Linlin Bao1,2, Wei Deng1,2, Baoying Huang3, Hong Gao1,2, Jiangning Liu1,2, Lili Ren4, Qiang Wei1,2, Pin Yu1,2, Yanfeng Xu1,2, Feifei Qi1,2, Yajin Qu1,2, Fengdi Li1,2, Qi Lv1,2, Wenling Wang3, Jing Xue1,2, Shuran Gong1,2, Mingya Liu1,2, Guanpeng Wang1,2, Shunyi Wang1,2, Zhiqi Song1,2, Linna Zhao1,2, Peipei Liu3, Li Zhao3, Fei Ye3, Huijuan Wang3, Weimin Zhou3, Na Zhu3, Wei Zhen3, Haisheng Yu1,2, Xiaojuan Zhang1,2, Li Guo4, Lan Chen4, Conghui Wang4, Ying Wang4, Xinming Wang4, Yan Xiao4, Qiangming Sun5, Hongqi Liu5, Fanli Zhu5, Chunxia Ma5, Lingmei Yan5, Mengli Yang5, Jun Han3, Wenbo Xu3, Wenjie Tan3, Xiaozhong Peng5, Qi Jin4, Guizhen Wu6, Chuan Qin7,8.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease 2019 (COVID-19), which has become a public health emergency of international concern1. Angiotensin-converting enzyme 2 (ACE2) is the cell-entry receptor for severe acute respiratory syndrome coronavirus (SARS-CoV)2. Here we infected transgenic mice that express human ACE2 (hereafter, hACE2 mice) with SARS-CoV-2 and studied the pathogenicity of the virus. We observed weight loss as well as virus replication in the lungs of hACE2 mice infected with SARS-CoV-2. The typical histopathology was interstitial pneumonia with infiltration of considerable numbers of macrophages and lymphocytes into the alveolar interstitium, and the accumulation of macrophages in alveolar cavities. We observed viral antigens in bronchial epithelial cells, macrophages and alveolar epithelia. These phenomena were not found in wild-type mice infected with SARS-CoV-2. Notably, we have confirmed the pathogenicity of SARS-CoV-2 in hACE2 mice. This mouse model of SARS-CoV-2 infection will be valuable for evaluating antiviral therapeutic agents and vaccines, as well as understanding the pathogenesis of COVID-19.Entities:
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Year: 2020 PMID： 32380511 DOI： 10.1038/s41586-020-2312-y
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 49.962