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Redox Homeostasis and Immune Alterations in Coronavirus Disease-19

SIMPLE SUMMARY: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has caused the Coronavirus Disease 2019 (COVID-19) pandemic, which may present with a wide clinical presentation. The capability of preventing serious illness with early interventions or managing severe disease is of extrem...

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Autores principales: Bellanti, Francesco, Lo Buglio, Aurelio, Vendemiale, Gianluigi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8869285/
https://www.ncbi.nlm.nih.gov/pubmed/35205026
http://dx.doi.org/10.3390/biology11020159
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author Bellanti, Francesco
Lo Buglio, Aurelio
Vendemiale, Gianluigi
author_facet Bellanti, Francesco
Lo Buglio, Aurelio
Vendemiale, Gianluigi
author_sort Bellanti, Francesco
collection PubMed
description SIMPLE SUMMARY: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has caused the Coronavirus Disease 2019 (COVID-19) pandemic, which may present with a wide clinical presentation. The capability of preventing serious illness with early interventions or managing severe disease is of extreme importance, encouraging the search for therapeutic targets. We review current evidence on the involvement of oxidant molecules with severe infection and lung injury in COVID-19. Reactive species and redox imbalance may dysregulate the immune response and account for disease progression in SARS-CoV-2 infection. This aspect suggests treatment options that could hinder disease progression and prevent multiple features of severe illness, which include clotting predisposition, cytokine storm and organ damage. ABSTRACT: The global Coronavirus Disease 2019 (COVID-19) pandemic is characterized by a wide variety of clinical features, from no or moderate symptoms to severe illness. COVID-19 is caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that first affects the respiratory tract. Other than being limited to lungs, SARS-CoV-2 may lead to a multisystem disease that can even be durable (long COVID). The clinical spectrum of COVID-19 depends on variability in the immune regulation. Indeed, disease progression is consequent to failure in the immune regulation, characterized by an intensification of the pro-inflammatory response. Disturbance of systemic and organ-related redox balance may be a further mechanism underlying variability in COVID-19 severity. Other than being determinant for SARS-CoV-2 entry and fusion to the host cell, reactive species and redox signaling are deeply involved in the immune response. This review sums up the present knowledge on the role of redox balance in the regulation of susceptibility to SARS-CoV-2 infection and related immune response, debating the effectiveness of antioxidant compounds in the management of COVID-19.
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spelling pubmed-88692852022-02-25 Redox Homeostasis and Immune Alterations in Coronavirus Disease-19 Bellanti, Francesco Lo Buglio, Aurelio Vendemiale, Gianluigi Biology (Basel) Review SIMPLE SUMMARY: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has caused the Coronavirus Disease 2019 (COVID-19) pandemic, which may present with a wide clinical presentation. The capability of preventing serious illness with early interventions or managing severe disease is of extreme importance, encouraging the search for therapeutic targets. We review current evidence on the involvement of oxidant molecules with severe infection and lung injury in COVID-19. Reactive species and redox imbalance may dysregulate the immune response and account for disease progression in SARS-CoV-2 infection. This aspect suggests treatment options that could hinder disease progression and prevent multiple features of severe illness, which include clotting predisposition, cytokine storm and organ damage. ABSTRACT: The global Coronavirus Disease 2019 (COVID-19) pandemic is characterized by a wide variety of clinical features, from no or moderate symptoms to severe illness. COVID-19 is caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that first affects the respiratory tract. Other than being limited to lungs, SARS-CoV-2 may lead to a multisystem disease that can even be durable (long COVID). The clinical spectrum of COVID-19 depends on variability in the immune regulation. Indeed, disease progression is consequent to failure in the immune regulation, characterized by an intensification of the pro-inflammatory response. Disturbance of systemic and organ-related redox balance may be a further mechanism underlying variability in COVID-19 severity. Other than being determinant for SARS-CoV-2 entry and fusion to the host cell, reactive species and redox signaling are deeply involved in the immune response. This review sums up the present knowledge on the role of redox balance in the regulation of susceptibility to SARS-CoV-2 infection and related immune response, debating the effectiveness of antioxidant compounds in the management of COVID-19. MDPI 2022-01-19 /pmc/articles/PMC8869285/ /pubmed/35205026 http://dx.doi.org/10.3390/biology11020159 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Bellanti, Francesco
Lo Buglio, Aurelio
Vendemiale, Gianluigi
Redox Homeostasis and Immune Alterations in Coronavirus Disease-19
title Redox Homeostasis and Immune Alterations in Coronavirus Disease-19
title_full Redox Homeostasis and Immune Alterations in Coronavirus Disease-19
title_fullStr Redox Homeostasis and Immune Alterations in Coronavirus Disease-19
title_full_unstemmed Redox Homeostasis and Immune Alterations in Coronavirus Disease-19
title_short Redox Homeostasis and Immune Alterations in Coronavirus Disease-19
title_sort redox homeostasis and immune alterations in coronavirus disease-19
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8869285/
https://www.ncbi.nlm.nih.gov/pubmed/35205026
http://dx.doi.org/10.3390/biology11020159
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