PT  - JOURNAL ARTICLE
AU  - Qing Ye
AU  - Jia Zhou
AU  - Guan Yang
AU  - Rui-Ting Li
AU  - Qi He
AU  - Yao Zhang
AU  - Shu-Jia Wu
AU  - Qi Chen
AU  - Jia-Hui Shi
AU  - Rong-Rong Zhang
AU  - Hui-Min Zhu
AU  - Hong-Ying Qiu
AU  - Tao Zhang
AU  - Yong-Qiang Deng
AU  - Xiao-Feng Li
AU  - Ping Xu
AU  - Xiao Yang
AU  - Cheng-Feng Qin
TI  - SARS-CoV-2 infection causes transient olfactory dysfunction in mice
AID  - 10.1101/2020.11.10.376673
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.11.10.376673
4099  - http://biorxiv.org/content/early/2020/11/10/2020.11.10.376673.short
4100  - http://biorxiv.org/content/early/2020/11/10/2020.11.10.376673.full
AB  - Olfactory dysfunction caused by SARS-CoV-2 infection represents as one of the most predictive and common symptoms in COVID-19 patients. However, the causal link between SARS-CoV-2 infection and olfactory disorders remains lacking. Herein we demonstrate intranasal inoculation of SARS-CoV-2 induces robust viral replication in the olfactory epithelium (OE), resulting in transient olfactory dysfunction in humanized ACE2 mice. The sustentacular cells and Bowman’s gland cells in OE were identified as the major targets of SARS-CoV-2 before the invasion into olfactory sensory neurons. Remarkably, SARS-CoV-2 infection triggers cell death and immune cell infiltration, and impairs the uniformity of OE structure. Combined transcriptomic and proteomic analyses reveal the induction of antiviral and inflammatory responses, as well as the downregulation of olfactory receptors in OE from the infected animals. Overall, our mouse model recapitulates the olfactory dysfunction in COVID-19 patients, and provides critical clues to understand the physiological basis for extrapulmonary manifestations of COVID-19.Competing Interest StatementThe authors have declared no competing interest.