The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis

Coronavirus Disease 2019 (COVID-19), caused by the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), persists as a threat to global health and continues to be a rapidly evolving condition. Although COVID19 is negatively correlated with the existing comorbidities in terms of the cl...

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Autores principales: Dženan Kovačić, Jovana Jotanović, Jasmina Laković
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Publicado: Poznan University of Medical Sciences 2021
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Acceso en línea:https://doaj.org/article/ef0e73cb198e4f488d507c7d6f051150
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spelling oai:doaj.org-article:ef0e73cb198e4f488d507c7d6f0511502021-11-11T08:05:30ZThe possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis10.20883/medical.e5602353-97982353-9801https://doaj.org/article/ef0e73cb198e4f488d507c7d6f0511502021-10-01T00:00:00Zhttps://jms.ump.edu.pl/index.php/JMS/article/view/560https://doaj.org/toc/2353-9798https://doaj.org/toc/2353-9801 Coronavirus Disease 2019 (COVID-19), caused by the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), persists as a threat to global health and continues to be a rapidly evolving condition. Although COVID19 is negatively correlated with the existing comorbidities in terms of the clinical outcome, the ability of SARS-CoV-2 to mediate the novel, or to exacerbate the existing autoimmune conditions, has generated considerable interest, due to its potential implications both with regard to patients suffering from autoimmune conditions, as well as to the long-term consequences of the disease. However, although molecular mimicry has been postulated as a potential causative factor in post-COVID19 autoimmunity and multi-organ damage, a substantial body of research needs to emerge in order to achieve a more definitive conclusion. We investigated the possibility of SARS-CoV-2 peptide sequences behaving as molecular mimics with a potential to trigger an autoimmune response. Thus, on the basis of analysis in silico, we were able to develop a plausible case for the molecular mimicry as a potential aetiological mechanism of SARS-CoV-2-mediated autoimmunity, both in a multi-organ damage context or outside of the viral phase of infection. Interestingly, this is the first time that the peptide sequence of MACROD1 has been implicated in the COVID-19 autoimmunity. Additionally, we also confirm that PARP9 and PARP14 may be involved in the process. Dženan KovačićJovana JotanovićJasmina LakovićPoznan University of Medical Sciencesarticleautoimmunity and COVID19molecular mimicry and COVID19SARS-CoV-2 autoimmunitymolecular mimicryMedicineRENJournal of Medical Science, Vol 90, Iss 3 (2021)
institution DOAJ
collection DOAJ
language EN
topic autoimmunity and COVID19
molecular mimicry and COVID19
SARS-CoV-2 autoimmunity
molecular mimicry
Medicine
R
spellingShingle autoimmunity and COVID19
molecular mimicry and COVID19
SARS-CoV-2 autoimmunity
molecular mimicry
Medicine
R
Dženan Kovačić
Jovana Jotanović
Jasmina Laković
The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis
description Coronavirus Disease 2019 (COVID-19), caused by the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), persists as a threat to global health and continues to be a rapidly evolving condition. Although COVID19 is negatively correlated with the existing comorbidities in terms of the clinical outcome, the ability of SARS-CoV-2 to mediate the novel, or to exacerbate the existing autoimmune conditions, has generated considerable interest, due to its potential implications both with regard to patients suffering from autoimmune conditions, as well as to the long-term consequences of the disease. However, although molecular mimicry has been postulated as a potential causative factor in post-COVID19 autoimmunity and multi-organ damage, a substantial body of research needs to emerge in order to achieve a more definitive conclusion. We investigated the possibility of SARS-CoV-2 peptide sequences behaving as molecular mimics with a potential to trigger an autoimmune response. Thus, on the basis of analysis in silico, we were able to develop a plausible case for the molecular mimicry as a potential aetiological mechanism of SARS-CoV-2-mediated autoimmunity, both in a multi-organ damage context or outside of the viral phase of infection. Interestingly, this is the first time that the peptide sequence of MACROD1 has been implicated in the COVID-19 autoimmunity. Additionally, we also confirm that PARP9 and PARP14 may be involved in the process.
format article
author Dženan Kovačić
Jovana Jotanović
Jasmina Laković
author_facet Dženan Kovačić
Jovana Jotanović
Jasmina Laković
author_sort Dženan Kovačić
title The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis
title_short The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis
title_full The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis
title_fullStr The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis
title_full_unstemmed The possible role of molecular mimicry in SARS-CoV-2-mediated autoimmunity: an immunobiochemical basis
title_sort possible role of molecular mimicry in sars-cov-2-mediated autoimmunity: an immunobiochemical basis
publisher Poznan University of Medical Sciences
publishDate 2021
url https://doaj.org/article/ef0e73cb198e4f488d507c7d6f051150
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