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SARS-CoV-2, Trait Anxiety, and the Microbiome

During the COVID-19 pandemic, research on the relationships between the virus and its human host has become fundamental to understand this pathology and its effects. Attaining this profound understanding is critical for the effective containment and treatment of infections caused by the virus. In th...

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Autores principales: Büttiker, Pascal, Weissenberger, Simon, Stefano, George B., Kream, Richard M., Ptacek, Radek
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8455943/
https://www.ncbi.nlm.nih.gov/pubmed/34566721
http://dx.doi.org/10.3389/fpsyt.2021.720082
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author Büttiker, Pascal
Weissenberger, Simon
Stefano, George B.
Kream, Richard M.
Ptacek, Radek
author_facet Büttiker, Pascal
Weissenberger, Simon
Stefano, George B.
Kream, Richard M.
Ptacek, Radek
author_sort Büttiker, Pascal
collection PubMed
description During the COVID-19 pandemic, research on the relationships between the virus and its human host has become fundamental to understand this pathology and its effects. Attaining this profound understanding is critical for the effective containment and treatment of infections caused by the virus. In this review, we present some possible mechanisms by which psychopathological symptoms emerge following viral infections of the central nervous system (CNS). These proposed mechanisms are based on microbial communication and the induced priming of microglial antibody activation within the CNS through Toll-like receptor signaling. In this process, chronic microglial activation causes increased glutamate release in virally-altered, high-density neuronal structures, thereby modulating cognitive networks and information integration processes. This modulation, in turn, we suggest, affects the accuracy of sensory integration and connectivity of major control networks, such as the default mode network. The chronic activation of immunological responses and neurochemical shifts toward an elevated glutamate/gamma-aminobutyric acid ratio lead to negative reinforcement learning and suboptimal organismic functioning, for example, maintaining the body in an anxious state, which can later become internalized as trait anxiety. Therefore, we hypothesize that the homeostatic relationship between host, microbiome, and virome, would be decisive in determining the efficiency of subsequent immunological responses, disease susceptibility, and long-term psychopathological effects of diseases that impact the CNS, such as the COVID-19.
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spelling pubmed-84559432021-09-23 SARS-CoV-2, Trait Anxiety, and the Microbiome Büttiker, Pascal Weissenberger, Simon Stefano, George B. Kream, Richard M. Ptacek, Radek Front Psychiatry Psychiatry During the COVID-19 pandemic, research on the relationships between the virus and its human host has become fundamental to understand this pathology and its effects. Attaining this profound understanding is critical for the effective containment and treatment of infections caused by the virus. In this review, we present some possible mechanisms by which psychopathological symptoms emerge following viral infections of the central nervous system (CNS). These proposed mechanisms are based on microbial communication and the induced priming of microglial antibody activation within the CNS through Toll-like receptor signaling. In this process, chronic microglial activation causes increased glutamate release in virally-altered, high-density neuronal structures, thereby modulating cognitive networks and information integration processes. This modulation, in turn, we suggest, affects the accuracy of sensory integration and connectivity of major control networks, such as the default mode network. The chronic activation of immunological responses and neurochemical shifts toward an elevated glutamate/gamma-aminobutyric acid ratio lead to negative reinforcement learning and suboptimal organismic functioning, for example, maintaining the body in an anxious state, which can later become internalized as trait anxiety. Therefore, we hypothesize that the homeostatic relationship between host, microbiome, and virome, would be decisive in determining the efficiency of subsequent immunological responses, disease susceptibility, and long-term psychopathological effects of diseases that impact the CNS, such as the COVID-19. Frontiers Media S.A. 2021-09-08 /pmc/articles/PMC8455943/ /pubmed/34566721 http://dx.doi.org/10.3389/fpsyt.2021.720082 Text en Copyright © 2021 Büttiker, Weissenberger, Stefano, Kream and Ptacek. 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 Psychiatry
Büttiker, Pascal
Weissenberger, Simon
Stefano, George B.
Kream, Richard M.
Ptacek, Radek
SARS-CoV-2, Trait Anxiety, and the Microbiome
title SARS-CoV-2, Trait Anxiety, and the Microbiome
title_full SARS-CoV-2, Trait Anxiety, and the Microbiome
title_fullStr SARS-CoV-2, Trait Anxiety, and the Microbiome
title_full_unstemmed SARS-CoV-2, Trait Anxiety, and the Microbiome
title_short SARS-CoV-2, Trait Anxiety, and the Microbiome
title_sort sars-cov-2, trait anxiety, and the microbiome
topic Psychiatry
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8455943/
https://www.ncbi.nlm.nih.gov/pubmed/34566721
http://dx.doi.org/10.3389/fpsyt.2021.720082
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