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Visualizing in deceased COVID-19 patients how SARS-CoV-2 attacks the respiratory and olfactory mucosae but spares the olfactory bulbopen access

Authors
Khan, MonaYoo, Seung JunClijsters, MarnickBackaert, WoutVanstapel, ArnoSpeleman, KatoLietaer, CharlotteChoi, SuminHether, Tyler D.Marcelis, LukasNam, AndrewPan, LiuliuReeves, Jason W.Van Bulck, PaulineZhou, HaiBourgeois, MarcDebaveye, YvesDe Munter, PaulGunst, JanJorissen, MarkLagrou, KatrienLorent, NatalieNeyrinck, ArnePeetermans, MarijkeThal, Dietmar RudolfVandenbriele, ChristopheWauters, JoostMombaerts, PeterVan Gerven, Laura
Issue Date
Nov-2021
Publisher
CELL PRESS
Citation
CELL, v.184, no.24, pp.5932 - 5949.e15
Indexed
SCIE
SCOPUS
Journal Title
CELL
Volume
184
Number
24
Start Page
5932
End Page
5949.e15
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/189206
DOI
10.1016/j.cell.2021.10.027
ISSN
0092-8674
Abstract
Anosmia, the loss of smell, is a common and often the sole symptom of COVID-19. The onset of the sequence of pathobiological events leading to olfactory dysfunction remains obscure. Here, we have developed a postmortem bedside surgical procedure to harvest endoscopically samples of respiratory and olfactory mucosae and whole olfactory bulbs. Our cohort of 85 cases included COVID-19 patients who died a few days after infection with SARS-CoV-2, enabling us to catch the virus while it was still replicating. We found that sustentacular cells are the major target cell type in the olfactory mucosa. We failed to find evidence for infection of olfactory sensory neurons, and the parenchyma of the olfactory bulb is spared as well. Thus, SARS-CoV-2 does not appear to be a neurotropic virus. We postulate that transient insufficient support from sustentacular cells triggers transient olfactory dysfunction in COVID-19. Olfactory sensory neurons would become affected without getting infected.
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서울 자연과학대학 > 서울 생명과학과 > 1. Journal Articles

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