Mary Wilson
Well-known member
This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published
in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Published:November 02, 2021
Accepted: October 25, 2021
DOI: https://doi.org/10.1016/j.cell.2021.10.027
Mona Khan, Seung-Jun Yoo, Marnick Clijsters, Wout Backaert, Arno Vanstapel, Kato Speleman, Charlotte Lietaer, Sumin Choi, Tyler D. Hether, Lukas Marcelis, Andrew Nam, Liuliu Pan, Jason W. Reeves, Pauline Van Bulck, Hai Zhou, Marc Bourgeois, Yves Debaveye, Paul De Munter, Jan Gunst, Mark Jorissen, Katrien Lagrou, Natalie Lorent, Arne Neyrinck, Marijke Peetermans, Dietmar Rudolf Thal, Christophe Vandenbriele, Joost Wauters, Peter Mombaerts, Laura Van Gerven
Highlights
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.
https://www.cell.com/action/showPdf?pii=S0092-8674(21)01282-4
in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Published:November 02, 2021
Accepted: October 25, 2021
DOI: https://doi.org/10.1016/j.cell.2021.10.027
Mona Khan, Seung-Jun Yoo, Marnick Clijsters, Wout Backaert, Arno Vanstapel, Kato Speleman, Charlotte Lietaer, Sumin Choi, Tyler D. Hether, Lukas Marcelis, Andrew Nam, Liuliu Pan, Jason W. Reeves, Pauline Van Bulck, Hai Zhou, Marc Bourgeois, Yves Debaveye, Paul De Munter, Jan Gunst, Mark Jorissen, Katrien Lagrou, Natalie Lorent, Arne Neyrinck, Marijke Peetermans, Dietmar Rudolf Thal, Christophe Vandenbriele, Joost Wauters, Peter Mombaerts, Laura Van Gerven
Highlights
- Postmortem bedside surgical procedure was developed for COVID-19 and control patients
- Ciliated cells are the main target cell type for SARS-CoV-2 in respiratory mucosa
- Sustentacular cells (non-neuronal) are the main target cell type in olfactory mucosa
- No evidence for infection of olfactory sensory neurons or olfactory bulb parenchyma
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.
https://www.cell.com/action/showPdf?pii=S0092-8674(21)01282-4
