The pathogenicity of SARS-CoV-2 in hACE2 transgenic mice.
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Bao Linlin, Deng Wei, Huang Baoying, Gao Hong, Liu Jiangning, Ren Lili, Wei Qiang, Yu Pin, Xu Yanfeng, Qi Feifei, Qu Yajin, Li Fengdi, Lv Qi, Wang Wenling, Xue Jing, Gong Shuran, Liu Mingya, Wang Guanpeng, Wang Shunyi, Song Zhiqi, Zhao Linna, Liu Peipei, Zhao Li, Ye Fei, Wang Huijuan, Zhou Weimin, Zhu Na, Zhen Wei, Yu Haisheng, Zhang Xiaojuan, Guo Li, Chen Lan, Wang Conghui, Wang Ying, Wang Xinming, Xiao Yan, Sun Qiangming, Liu Hongqi, Zhu Fanli, Ma Chunxia, Yan Lingmei, Yang Mengli, Han Jun, Xu Wenbo, Tan Wenjie, Peng Xiaozhong, Jin Qi, Wu Guizhen, Qin Chuan
Аннотация
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.