Cell · 2022
Non-cell-autonomous disruption of nuclear architecture as a potential cause of COVID-19-induced anosmia.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zazhytska Marianna, Kodra Albana, Hoagland Daisy A, Frere Justin, Fullard John F, Shayya Hani, McArthur Natalie G, Moeller Rasmus, Uhl Skyler, Omer Arina D, Gottesman Max E, Firestein Stuart, Gong Qizhi, Canoll Peter D, Goldman James E, Roussos Panos, tenOever Benjamin R, Jonathan B Overdevest, Lomvardas Stavros
Аннотация
SARS-CoV-2 infects less than 1% of cells in the human body, yet it can cause severe damage in a variety of organs. Thus, deciphering the non-cell-autonomous effects of SARS-CoV-2 infection is imperative for understanding the cellular and molecular disruption it elicits. Neurological and cognitive defects are among the least understood symptoms of COVID-19 patients, with olfactory dysfunction being their most common sensory deficit. Here, we show that both in humans and hamsters, SARS-CoV-2 infection causes widespread downregulation of olfactory receptors (ORs) and of their signaling components. This non-cell-autonomous effect is preceded by a dramatic reorganization of the neuronal nuclear architecture, which results in dissipation of genomic compartments harboring OR genes. Our data provide a potential mechanism by which SARS-CoV-2 infection alters the cellular morphology and the transcriptome of cells it cannot infect, offering insight to its systemic effects in olfaction and beyond.