Science advances · 2020
Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАПоддержка правительства СШАНазвание и аннотация: Перевод в очереди
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Brann David H, Tsukahara Tatsuya, Weinreb Caleb, Lipovsek Marcela, Van den Berge Koen, Gong Boying, Chance Rebecca, Macaulay Iain C, Chou Hsin-Jung, Fletcher Russell B, Das Diya, Street Kelly, de Bezieux Hector Roux, Choi Yoon-Gi, Risso Davide, Dudoit Sandrine, Purdom Elizabeth, Mill Jonathan, Hachem Ralph Abi, Matsunami Hiroaki, Logan Darren W, Goldstein Bradley J, Grubb Matthew S, Ngai John, Datta Sandeep Robert
Аннотация
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 demonstrated 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 revealed that ACE2 is expressed in support cells, stem cells, and perivascular cells, rather than in neurons. Immunostaining confirmed these results and revealed pervasive expression of ACE2 protein in dorsally-located olfactory epithelial sustentacular cells and olfactory bulb pericytes in the mouse. 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.