Cell · 2021
Visualizing in deceased COVID-19 patients how SARS-CoV-2 attacks the respiratory and olfactory mucosae but spares the olfactory bulb.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Khan Mona, Yoo Seung-Jun, Clijsters Marnick, Backaert Wout, Vanstapel Arno, Speleman Kato, Lietaer Charlotte, Choi Sumin, Hether Tyler D, Marcelis Lukas, Nam Andrew, Pan Liuliu, Reeves Jason W, Van Bulck Pauline, Zhou Hai, Bourgeois Marc, Debaveye Yves, De Munter Paul, Gunst Jan, Jorissen Mark, Lagrou Katrien, Lorent Natalie, Neyrinck Arne, Peetermans Marijke, Thal Dietmar Rudolf, Vandenbriele Christophe, Wauters Joost, Mombaerts Peter, Van Gerven Laura
Аннотация
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.