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COVID, complement, and the brain
The brains of COVID-19 patients are affected by the SARS-CoV-2 virus, and these effects may contribute to several COVID-19 sequelae, including cognitive dysfunction (termed “long COVID” by some researchers). Recent advances concerning the role of neuroinflammation and the consequences for brain func...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10391634/ https://www.ncbi.nlm.nih.gov/pubmed/37533859 http://dx.doi.org/10.3389/fimmu.2023.1216457 |
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author | Vlaicu, Sonia I. Tatomir, Alexandru Cuevas, Jacob Rus, Violeta Rus, Horea |
author_facet | Vlaicu, Sonia I. Tatomir, Alexandru Cuevas, Jacob Rus, Violeta Rus, Horea |
author_sort | Vlaicu, Sonia I. |
collection | PubMed |
description | The brains of COVID-19 patients are affected by the SARS-CoV-2 virus, and these effects may contribute to several COVID-19 sequelae, including cognitive dysfunction (termed “long COVID” by some researchers). Recent advances concerning the role of neuroinflammation and the consequences for brain function are reviewed in this manuscript. Studies have shown that respiratory SARS-CoV-2 infection in mice and humans is associated with selective microglial reactivity in the white matter, persistently impaired hippocampal neurogenesis, a decrease in the number of oligodendrocytes, and myelin loss. Brain MRI studies have revealed a greater reduction in grey matter thickness in the orbitofrontal cortex and parahippocampal gyrus, associated with a greater reduction in global brain size, in those with SARS-CoV-2 and a greater cognitive decline. COVID-19 can directly infect endothelial cells of the brain, potentially promoting clot formation and stroke; complement C3 seems to play a major role in this process. As compared to controls, the brain tissue of patients who died from COVID-19 have shown a significant increase in the extravasation of fibrinogen, indicating leakage in the blood–brain barrier; furthermore, recent studies have documented the presence of IgG, IgM, C1q, C4d, and C5b-9 deposits in the brain tissue of COVID-19 patients. These data suggest an activation of the classical complement pathway and an immune-mediated injury to the endothelial cells. These findings implicate both the classical and alternative complement pathways, and they indicate that C3b and the C5b-9 terminal complement complex (membrane attack complex, MAC) are acting in concert with neuroinflammatory and immune factors to contribute to the neurological sequelae seen in patients with COVID. |
format | Online Article Text |
id | pubmed-10391634 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-103916342023-08-02 COVID, complement, and the brain Vlaicu, Sonia I. Tatomir, Alexandru Cuevas, Jacob Rus, Violeta Rus, Horea Front Immunol Immunology The brains of COVID-19 patients are affected by the SARS-CoV-2 virus, and these effects may contribute to several COVID-19 sequelae, including cognitive dysfunction (termed “long COVID” by some researchers). Recent advances concerning the role of neuroinflammation and the consequences for brain function are reviewed in this manuscript. Studies have shown that respiratory SARS-CoV-2 infection in mice and humans is associated with selective microglial reactivity in the white matter, persistently impaired hippocampal neurogenesis, a decrease in the number of oligodendrocytes, and myelin loss. Brain MRI studies have revealed a greater reduction in grey matter thickness in the orbitofrontal cortex and parahippocampal gyrus, associated with a greater reduction in global brain size, in those with SARS-CoV-2 and a greater cognitive decline. COVID-19 can directly infect endothelial cells of the brain, potentially promoting clot formation and stroke; complement C3 seems to play a major role in this process. As compared to controls, the brain tissue of patients who died from COVID-19 have shown a significant increase in the extravasation of fibrinogen, indicating leakage in the blood–brain barrier; furthermore, recent studies have documented the presence of IgG, IgM, C1q, C4d, and C5b-9 deposits in the brain tissue of COVID-19 patients. These data suggest an activation of the classical complement pathway and an immune-mediated injury to the endothelial cells. These findings implicate both the classical and alternative complement pathways, and they indicate that C3b and the C5b-9 terminal complement complex (membrane attack complex, MAC) are acting in concert with neuroinflammatory and immune factors to contribute to the neurological sequelae seen in patients with COVID. Frontiers Media S.A. 2023-07-18 /pmc/articles/PMC10391634/ /pubmed/37533859 http://dx.doi.org/10.3389/fimmu.2023.1216457 Text en Copyright © 2023 Vlaicu, Tatomir, Cuevas, Rus and Rus https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Vlaicu, Sonia I. Tatomir, Alexandru Cuevas, Jacob Rus, Violeta Rus, Horea COVID, complement, and the brain |
title | COVID, complement, and the brain |
title_full | COVID, complement, and the brain |
title_fullStr | COVID, complement, and the brain |
title_full_unstemmed | COVID, complement, and the brain |
title_short | COVID, complement, and the brain |
title_sort | covid, complement, and the brain |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10391634/ https://www.ncbi.nlm.nih.gov/pubmed/37533859 http://dx.doi.org/10.3389/fimmu.2023.1216457 |
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