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Comment
. 2022 May 9;57(9):1081-1082.
doi: 10.1016/j.devcel.2022.04.015.

Can't smell the virus: SARS-CoV-2, chromatin organization, and anosmia

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Comment

Can't smell the virus: SARS-CoV-2, chromatin organization, and anosmia

Matan Sorek et al. Dev Cell. .

Abstract

Anosmia, or loss of smell, is strongly associated with SARS-CoV-2 infection in humans, but the underlying mechanism remains obscure. In a recent Cell study, Zazhytska et al. (2022) report non-cell-autonomous disruption of long-range genomic interactions of olfactory receptor genes in response to SARS-CoV-2 infection, and these interactions remain disrupted long after virus clearance.

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Conflict of interest statement

Declaration of interests The authors declare no competing interests.

Figures

Figure 1
Figure 1
SARS-CoV-2 infection leads to non-cell-autonomous genome rearrangement in olfactory sensory neurons (A) Olfactory sensory neurons (OSNs) have a typical “fried-egg”-like nuclear conformation in which large chromatin domains are clustered around the center of the nucleus. This unique chromatin organization ensures both silencing via juxtaposition to heterochromatin and activation through mediating long-range enhancer-promoter interactions, e.g. of the Adcy3 gene (inset). (B) Upon SARS-CoV-2 infection of neighboring sustentacular (SUS) cells, global rearrangement of chromatin in OSNs leads to disruption of long-range interactions between enhancers (green) and promoters (yellow) and to the down-regulation of OR-related genes.

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