Non-cell-autonomous disruption of nuclear architecture as a potential cause of COVID-19-induced anosmia.
Cell
; 185(6): 1052-1064.e12, 2022 03 17.
Article
em En
| MEDLINE
| ID: mdl-35180380
ABSTRACT
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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Base de dados:
MEDLINE
Assunto principal:
Anosmia
/
COVID-19
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article