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Neuropathobiology of COVID-19 : The Role for Glia Tremblay, Marie-Ève (Neuroscientist); Madore, Charlotte; Bordeleau, Maude; Tian, Li; Verkhratsky, Alexei

Abstract

SARS-CoV-2, which causes the Coronavirus Disease 2019 (COVID-19) pandemic, has a brain neurotropism through binding to the receptor angiotensin-converting enzyme 2 expressed by neurones and glial cells, including astrocytes and microglia. Systemic infection which accompanies severe cases of COVID-19 also triggers substantial increase in circulating levels of chemokines and interleukins that compromise the blood-brain barrier, enter the brain parenchyma and affect its defensive systems, astrocytes and microglia. Brain areas devoid of a blood-brain barrier such as the circumventricular organs are particularly vulnerable to circulating inflammatory mediators. The performance of astrocytes and microglia, as well as of immune cells required for brain health, is considered critical in defining the neurological damage and neurological outcome of COVID-19. In this review, we discuss the neurotropism of SARS-CoV-2, the implication of neuroinflammation, adaptive and innate immunity, autoimmunity, as well as astrocytic and microglial immune and homeostatic functions in the neurological and psychiatric aspects of COVID-19. The consequences of SARS-CoV-2 infection during ageing, in the presence of systemic comorbidities, and for the exposed pregnant mother and foetus are also covered.

Item Metadata

Title
Neuropathobiology of COVID-19 : The Role for Glia
Creator
Tremblay, Marie-Ève (Neuroscientist); Madore, Charlotte; Bordeleau, Maude; Tian, Li; Verkhratsky, Alexei
Publisher
Frontiers
Date Issued
2020-11-11
Description
SARS-CoV-2, which causes the Coronavirus Disease 2019 (COVID-19) pandemic, has a brain neurotropism through binding to the receptor angiotensin-converting enzyme 2 expressed by neurones and glial cells, including astrocytes and microglia. Systemic infection which accompanies severe cases of COVID-19 also triggers substantial increase in circulating levels of chemokines and interleukins that compromise the blood-brain barrier, enter the brain parenchyma and affect its defensive systems, astrocytes and microglia. Brain areas devoid of a blood-brain barrier such as the circumventricular organs are particularly vulnerable to circulating inflammatory mediators. The performance of astrocytes and microglia, as well as of immune cells required for brain health, is considered critical in defining the neurological damage and neurological outcome of COVID-19. In this review, we discuss the neurotropism of SARS-CoV-2, the implication of neuroinflammation, adaptive and innate immunity, autoimmunity, as well as astrocytic and microglial immune and homeostatic functions in the neurological and psychiatric aspects of COVID-19. The consequences of SARS-CoV-2 infection during ageing, in the presence of systemic comorbidities, and for the exposed pregnant mother and foetus are also covered.
Subject
COVID-19; SARS-CoV-2; immunity; astrocyte; microglia; ageing; comorbidity; development
Genre
Article
Type
Text
Language
eng
Date Available
2021-01-05
Provider
Vancouver : University of British Columbia Library
Rights
Attribution-NonCommercial-NoDerivatives 4.0 International
DOI
10.14288/1.0395449
URI
http://hdl.handle.net/2429/76946
Affiliation
Medicine, Faculty of; Non UBC; Biochemistry and Molecular Biology, Department of
Citation
Tremblay M-E, Madore C, Bordeleau M, Tian L and Verkhratsky A (2020) Neuropathobiology of COVID-19: The Role for Glia. Front. Cell. Neurosci. 14:592214.
Publisher DOI
10.3389/fncel.2020.592214
Peer Review Status
Reviewed
Scholarly Level
Faculty; Researcher
Copyright Holder
Authors
Rights URI
http://creativecommons.org/licenses/by-nc-nd/4.0/
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Attribution-NonCommercial-NoDerivatives 4.0 International