Abstract
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 Statement
DL is an employee of Mars, Inc. None of the other authors have competing interests to declare.
Footnotes
Includes previously unpublished datasets (whole olfactory mucosa scSeq, HBC scSeq, olfactory bulb scSeq, olfactory bulb dopaminergic neuron deep sequencing), ACE2 immunohistochemistry in human tissue, and analysis of SARS-CoV-2 cell entry genes in the olfactory bulb and brain; research groups of John Ngai, Matthew Grubb, Bradley Goldstein, Hiro Matsunami (and colleagues) added as collaborators.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4680959/bin/srep18178-s2.xls
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE139522
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE120199
