Non-cell-autonomous disruption of nuclear architecture as a potential cause of COVID-19-induced anosmia | Zendy

Marianna Zazhytska | Zendy; Albana Kodra | Zendy; Daisy A. Hoagland | Zendy; Justin J. Frere | Zendy; John F. Fullard | Zendy; Hani Shayya | Zendy; Natalie G. McArthur | Zendy; Rasmus Møeller | Zendy; Skyler Uhl | Zendy; Arina D. Omer | Zendy; Max E. Gottesman | Zendy; Stuart Firestein | Zendy; Qizhi Gong | Zendy; Peter Canoll | Zendy; James E. Goldman | Zendy; Panos Roussos | Zendy; Benjamin R. tenOever | Zendy; Jonathan B. Overdevest | Zendy; Stavros Lomvardas | Zendy

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Non-cell-autonomous disruption of nuclear architecture as a potential cause of COVID-19-induced anosmia

Author(s) -

Marianna Zazhytska,

Albana Kodra,

Daisy A. Hoagland,

Justin J. Frere,

John F. Fullard,

Hani Shayya,

Natalie G. McArthur,

Rasmus Møeller,

Skyler Uhl,

Arina D. Omer,

Max E. Gottesman,

Stuart Firestein,

Qizhi Gong,

Peter Canoll,

James E. Goldman,

Panos Roussos,

Benjamin R. tenOever,

Jonathan B. Overdevest,

Stavros Lomvardas

Publication year - 2022

Publication title -

cell

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 26.304

H-Index - 776

eISSN - 1097-4172

pISSN - 0092-8674

DOI - 10.1016/j.cell.2022.01.024

Subject(s) - biology , anosmia , olfaction , transcriptome , neuroscience , mechanism (biology) , downregulation and upregulation , olfactory system , sensory system , cell , covid-19 , microbiology and biotechnology , gene , disease , genetics , pathology , gene expression , medicine , philosophy , epistemology , infectious disease (medical specialty)

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.

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