Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia
By
David H. Brann,
Tatsuya Tsukahara,
Caleb Weinreb,
Marcela Lipovsek,
Koen Van den Berge,
Boying Gong,
Rebecca Chance,
Iain C Macaulay,
Hsin-jung Chou,
Russell Fletcher,
Diya Das,
Kelly N Street,
Hector Roux de Bézieux,
Yoon-Gi Choi,
Davide Risso,
Sandrine Dudoit,
Elizabeth Purdom,
Jonathan S Mill,
Ralph Abi Hachem,
Hiroaki Matsunami,
Darren W. Logan,
Bradley J. Goldstein,
Matthew S Grubb,
John Ngai,
Sandeep Robert Datta
Posted 27 Mar 2020
bioRxiv DOI: 10.1101/2020.03.25.009084
(published DOI: 10.1126/sciadv.abc5801)
Altered olfactory function is a common symptom of COVID-19, but its etiology is unknown. A key question is whether SARS-CoV-2 (CoV-2) - the causal agent in COVID-19 - affects olfaction directly by infecting olfactory sensory neurons or their targets in the olfactory bulb, or indirectly, through perturbation of supporting cells. Here we identify cell types in the olfactory epithelium and olfactory bulb that express SARS-CoV-2 cell entry molecules. Bulk sequencing revealed that mouse, non-human primate and human olfactory mucosa expresses two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, single cell sequencing and immunostaining demonstrated ACE2 expression in support cells, stem cells, and perivascular cells; in contrast, neurons in both the olfactory epithelium and bulb did not express ACE2 message or protein. 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. ### Competing Interest Statement DL is an employee of Mars, Inc. None of the other authors have competing interests to declare.
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