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Does SARS-CoV-2 Trigger Stress-Induced Autoimmunity by Molecular Mimicry? A Hypothesis

Viruses can generate molecular mimicry phenomena within their hosts. Why should severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) not be considered one of these? Information in this short review suggests that it might be so and, thus, encourages research aiming at testing this possibility...

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Autores principales: Cappello, Francesco, Marino Gammazza, Antonella, Dieli, Francesco, Conway de Macario, Everly, Macario, Alberto JL
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7408943/
https://www.ncbi.nlm.nih.gov/pubmed/32610587
http://dx.doi.org/10.3390/jcm9072038
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author Cappello, Francesco
Marino Gammazza, Antonella
Dieli, Francesco
Conway de Macario, Everly
Macario, Alberto JL
author_facet Cappello, Francesco
Marino Gammazza, Antonella
Dieli, Francesco
Conway de Macario, Everly
Macario, Alberto JL
author_sort Cappello, Francesco
collection PubMed
description Viruses can generate molecular mimicry phenomena within their hosts. Why should severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) not be considered one of these? Information in this short review suggests that it might be so and, thus, encourages research aiming at testing this possibility. We propose, as a working hypothesis, that the virus induces antibodies and that some of them crossreact with host’s antigens, thus eliciting autoimmune phenomena with devasting consequences in various tissues and organs. If confirmed, by in vitro and in vivo tests, this could drive researchers to find effective treatments against the virus.
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spelling pubmed-74089432020-08-13 Does SARS-CoV-2 Trigger Stress-Induced Autoimmunity by Molecular Mimicry? A Hypothesis Cappello, Francesco Marino Gammazza, Antonella Dieli, Francesco Conway de Macario, Everly Macario, Alberto JL J Clin Med Commentary Viruses can generate molecular mimicry phenomena within their hosts. Why should severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) not be considered one of these? Information in this short review suggests that it might be so and, thus, encourages research aiming at testing this possibility. We propose, as a working hypothesis, that the virus induces antibodies and that some of them crossreact with host’s antigens, thus eliciting autoimmune phenomena with devasting consequences in various tissues and organs. If confirmed, by in vitro and in vivo tests, this could drive researchers to find effective treatments against the virus. MDPI 2020-06-29 /pmc/articles/PMC7408943/ /pubmed/32610587 http://dx.doi.org/10.3390/jcm9072038 Text en © 2020 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Commentary
Cappello, Francesco
Marino Gammazza, Antonella
Dieli, Francesco
Conway de Macario, Everly
Macario, Alberto JL
Does SARS-CoV-2 Trigger Stress-Induced Autoimmunity by Molecular Mimicry? A Hypothesis
title Does SARS-CoV-2 Trigger Stress-Induced Autoimmunity by Molecular Mimicry? A Hypothesis
title_full Does SARS-CoV-2 Trigger Stress-Induced Autoimmunity by Molecular Mimicry? A Hypothesis
title_fullStr Does SARS-CoV-2 Trigger Stress-Induced Autoimmunity by Molecular Mimicry? A Hypothesis
title_full_unstemmed Does SARS-CoV-2 Trigger Stress-Induced Autoimmunity by Molecular Mimicry? A Hypothesis
title_short Does SARS-CoV-2 Trigger Stress-Induced Autoimmunity by Molecular Mimicry? A Hypothesis
title_sort does sars-cov-2 trigger stress-induced autoimmunity by molecular mimicry? a hypothesis
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7408943/
https://www.ncbi.nlm.nih.gov/pubmed/32610587
http://dx.doi.org/10.3390/jcm9072038
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