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Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection

Immune homeostasis is disturbed during severe viral infections, which can lead to loss of tolerance to self-peptides and result in short- or long-term autoimmunity. Using publicly available transcriptomic datasets, we conducted an in-silico analyses to evaluate the expression levels of 52 autoantige...

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Autores principales: Saheb Sharif-Askari, Narjes, Saheb Sharif-Askari, Fatemeh, Ahmed, Samrein B. M., Hannawi, Suad, Hamoudi, Rifat, Hamid, Qutayba, Halwani, Rabih
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8278821/
https://www.ncbi.nlm.nih.gov/pubmed/34276672
http://dx.doi.org/10.3389/fimmu.2021.686462
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author Saheb Sharif-Askari, Narjes
Saheb Sharif-Askari, Fatemeh
Ahmed, Samrein B. M.
Hannawi, Suad
Hamoudi, Rifat
Hamid, Qutayba
Halwani, Rabih
author_facet Saheb Sharif-Askari, Narjes
Saheb Sharif-Askari, Fatemeh
Ahmed, Samrein B. M.
Hannawi, Suad
Hamoudi, Rifat
Hamid, Qutayba
Halwani, Rabih
author_sort Saheb Sharif-Askari, Narjes
collection PubMed
description Immune homeostasis is disturbed during severe viral infections, which can lead to loss of tolerance to self-peptides and result in short- or long-term autoimmunity. Using publicly available transcriptomic datasets, we conducted an in-silico analyses to evaluate the expression levels of 52 autoantigens, known to be associated with 24 autoimmune diseases, during SAR-CoV-2 infection. Seven autoantigens (MPO, PRTN3, PADI4, IFIH1, TRIM21, PTPRN2, and TSHR) were upregulated in whole blood samples. MPO and TSHR were overexpressed in both lung autopsies and whole blood tissue and were associated with more severe COVID-19. Neutrophil activation derived autoantigens (MPO, PRTN3, and PADI4) were prominently increased in blood of both SARS-CoV-1 and SARS-CoV-2 viral infections, while TSHR and PTPRN2 autoantigens were specifically increased in SARS-CoV-2. Using single-cell dataset from peripheral blood mononuclear cells (PBMCs), we observed an upregulation of MPO, PRTN3, and PADI4 autoantigens within the low-density neutrophil subset. To validate our in-silico analysis, we measured plasma protein levels of two autoantigens, MPO and PRTN3, in severe and asymptomatic COVID-19. The protein levels of these two autoantigens were significantly upregulated in more severe COVID-19 infections. In conclusion, the immunopathology and severity of COVID-19 could result in transient autoimmune activation. Longitudinal follow-up studies of confirmed cases of COVID-19 could determine the enduring effects of viral infection including development of autoimmune disease.
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spelling pubmed-82788212021-07-15 Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection Saheb Sharif-Askari, Narjes Saheb Sharif-Askari, Fatemeh Ahmed, Samrein B. M. Hannawi, Suad Hamoudi, Rifat Hamid, Qutayba Halwani, Rabih Front Immunol Immunology Immune homeostasis is disturbed during severe viral infections, which can lead to loss of tolerance to self-peptides and result in short- or long-term autoimmunity. Using publicly available transcriptomic datasets, we conducted an in-silico analyses to evaluate the expression levels of 52 autoantigens, known to be associated with 24 autoimmune diseases, during SAR-CoV-2 infection. Seven autoantigens (MPO, PRTN3, PADI4, IFIH1, TRIM21, PTPRN2, and TSHR) were upregulated in whole blood samples. MPO and TSHR were overexpressed in both lung autopsies and whole blood tissue and were associated with more severe COVID-19. Neutrophil activation derived autoantigens (MPO, PRTN3, and PADI4) were prominently increased in blood of both SARS-CoV-1 and SARS-CoV-2 viral infections, while TSHR and PTPRN2 autoantigens were specifically increased in SARS-CoV-2. Using single-cell dataset from peripheral blood mononuclear cells (PBMCs), we observed an upregulation of MPO, PRTN3, and PADI4 autoantigens within the low-density neutrophil subset. To validate our in-silico analysis, we measured plasma protein levels of two autoantigens, MPO and PRTN3, in severe and asymptomatic COVID-19. The protein levels of these two autoantigens were significantly upregulated in more severe COVID-19 infections. In conclusion, the immunopathology and severity of COVID-19 could result in transient autoimmune activation. Longitudinal follow-up studies of confirmed cases of COVID-19 could determine the enduring effects of viral infection including development of autoimmune disease. Frontiers Media S.A. 2021-06-30 /pmc/articles/PMC8278821/ /pubmed/34276672 http://dx.doi.org/10.3389/fimmu.2021.686462 Text en Copyright © 2021 Saheb Sharif-Askari, Saheb Sharif-Askari, Ahmed, Hannawi, Hamoudi, Hamid and Halwani 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
Saheb Sharif-Askari, Narjes
Saheb Sharif-Askari, Fatemeh
Ahmed, Samrein B. M.
Hannawi, Suad
Hamoudi, Rifat
Hamid, Qutayba
Halwani, Rabih
Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection
title Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection
title_full Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection
title_fullStr Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection
title_full_unstemmed Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection
title_short Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection
title_sort enhanced expression of autoantigens during sars-cov-2 viral infection
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8278821/
https://www.ncbi.nlm.nih.gov/pubmed/34276672
http://dx.doi.org/10.3389/fimmu.2021.686462
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