Author:
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
Abstract
AbstractSevere acute respiratory syndrome CoV-2 (SARS-CoV-2) caused the Corona Virus Disease 2019 (COVID-19) cases in China has become a public health emergency of international concern (PHEIC). Based on angiotensin converting enzyme 2 (ACE2) as cell entry receptor of SARS-CoV, we used the hACE2 transgenic mice infected with SARS-CoV-2 to study the pathogenicity of the virus. Weight loss and virus replication in lung were observed in hACE2 mice infected with SARS-CoV-2. The typical histopathology was interstitial pneumonia with infiltration of significant lymphocytes and monocytes in alveolar interstitium, and accumulation of macrophages in alveolar cavities. Viral antigens were observed in the bronchial epithelial cells, alveolar macrophages and alveolar epithelia. The phenomenon was not found in wild type mice with SARS-CoV-2 infection. The pathogenicity of SARS-CoV-2 in hACE2 mice was clarified and the Koch’s postulates were fulfilled as well, and the mouse model may facilitate the development of therapeutics and vaccines against SARS-CoV-2.
Publisher
Cold Spring Harbor Laboratory