Neuropathobiology of COVID-19: The Role for Glia
Front. Cell. Neurosci.. 2020-11-11; 14:
DOI: 10.3389/fncel.2020.592214
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Tremblay ME(1)(2)(3)(4)(5), Madore C(6), Bordeleau M(1)(2), Tian L(7)(8), Verkhratsky A(9)(10)(11).
Author information:
(1)Axe Neurosciences, Centre de Recherche du CHU de Québec, Université Laval, Québec City, QC, Canada.
(2)Neurology and Neurosurgery Department, McGill University, Montréal, QC, Canada.
(3)Department of Molecular Medicine, Université Laval, Québec City, QC, Canada.
(4)Division of Medical Sciences, University of Victoria, Victoria, BC, Canada.
(5)Department of Biochemistry and Molecular Biology, The University of British Columbia, Vancouver, BC, Canada.
(6)Univ. Bordeaux, INRAE, Bordeaux INP, NutriNeuro, UMR 1286, Bordeaux, France.
(7)Department of Physiology, Faculty of Medicine, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
(8)Psychiatry Research Centre, Peking University Health Science Center, Beijing Huilongguan Hospital, Beijing, China.
(9)Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
(10)Achucarro Center for Neuroscience, IKERBASQUE, Basque Foundation for Science, Bilbao, Spain.
(11)Department of Neurosciences, University of the Basque Country Universidad del País Vasco/Euskal Herriko Unibertsitatea, Leioa, Spain.
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.
Copyright © 2020 Tremblay, Madore, Bordeleau, Tian and Verkhratsky.