PT  - JOURNAL ARTICLE
AU  - David H. Brann
AU  - Tatsuya Tsukahara
AU  - Caleb Weinreb
AU  - Marcela Lipovsek
AU  - Koen Van den Berge
AU  - Boying Gong
AU  - Rebecca Chance
AU  - Iain C. Macaulay
AU  - Hsin-jung Chou
AU  - Russell Fletcher
AU  - Diya Das
AU  - Kelly Street
AU  - Hector Roux de Bezieux
AU  - Yoon-Gi Choi
AU  - Davide Risso
AU  - Sandrine Dudoit
AU  - Elizabeth Purdom
AU  - Jonathan S. Mill
AU  - Ralph Abi Hachem
AU  - Hiroaki Matsunami
AU  - Darren W. Logan
AU  - Bradley J. Goldstein
AU  - Matthew S. Grubb
AU  - John Ngai
AU  - Sandeep Robert Datta
TI  - Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia
AID  - 10.1101/2020.03.25.009084
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.03.25.009084
4099  - http://biorxiv.org/content/early/2020/04/09/2020.03.25.009084.short
4100  - http://biorxiv.org/content/early/2020/04/09/2020.03.25.009084.full
AB  - A subset of COVID-19 patients exhibit altered olfactory function. Here we analyze bulk and single cell RNA-Seq datasets to identify cell types in the olfactory epithelium and olfactory bulb that express cell entry molecules that mediate infection by SARS-CoV-2 (CoV-2), the causal agent in COVID-19. We find that samples from whole olfactory mucosa in species including mouse and human express two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, neither olfactory sensory neurons nor olfactory bulb neurons express these genes, which are instead expressed in support cells, stem cells, and perivascular cells. These findings suggest that CoV-2 infection of non-neuronal cell types leads to anosmia and related disturbances in odor perception in COVID-19 patients.One Sentence Summary Analysis of new and previously published single-cell sequencing datasets reveals that the SARS-CoV2 receptor ACE2 is expressed in olfactory support cells, stem cells and perivascular cells — but not in neurons — suggesting mechanisms through which the COVID-19 syndrome could lead to olfactory dysfunction.Competing Interest StatementDL is an employee of Mars, Inc. None of the other authors have competing interests to declare.