The molecular basis of loss of smell in 2019-nCoV infected individuals

Abstract

<title>Abstract</title> Among the prominent clinical symptoms such as fatigue, shortness of breath, fever, and cough, 2019-nCoV infected individuals often experience hyposmia/anosmia (decrease or loss of sense of smell). Angiotensin I Converting Enzyme 2 (ACE2), a key host receptor has now been established as an important moiety for the entry of 2019-nCoV into the host cells. A multitude of studies estimated the expression of <italic>ACE2</italic> in multiple organs including heart, kidney, intestines, lungs, buccal cavity, etc. The ongoing medical examinations and the autopsy reports of the diseased individuals strongly corroborate these organ/tissue-level molecular insights. Olfactory mucosa harbors multiple functionally distinct cell types. Zeroing in on the cell lineages that underpin infection associated loss of olfaction may provide new leads for diagnostics/clinical management of 2019-nCoV infected individuals. Our pointed bioinformatic analysis of single-cell expression profiles underscored selective expression of <italic>ACE2</italic> in a subset of horizontal basal cells (HBCs) and sustentacular cells (SUSs) of the olfactory mucosa in humans. Inspection of the <italic>ACE2</italic> levels in the olfactory mucosa of 4 additional mammalian species revealed comparable expression patterns, indicating the risk of olfactory dysfunction in these species. In summary, our findings pinpoint the molecular rationale of loss of smell in 2019-nCoV infected patients.