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SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II
Patients infected with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can experience life-threatening respiratory distress, blood pressure dysregulation and thrombosis. This is thought to be associated with an impaired activity of angiotensin-converting enzyme-2 (ACE-2), which is t...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cold Spring Harbor Laboratory
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8575143/ https://www.ncbi.nlm.nih.gov/pubmed/34751272 http://dx.doi.org/10.1101/2021.11.02.21265789 |
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author | Briquez, Priscilla S. Rouhani, Sherin J. Yu, Jovian Pyzer, Athalia R. Trujillo, Jonathan Dugan, Haley L. Stamper, Christopher T. Changrob, Siriruk Sperling, Anne I. Wilson, Patrick C. Gajewski, Thomas F. Hubbell, Jeffrey A. Swartz, Melody A. |
author_facet | Briquez, Priscilla S. Rouhani, Sherin J. Yu, Jovian Pyzer, Athalia R. Trujillo, Jonathan Dugan, Haley L. Stamper, Christopher T. Changrob, Siriruk Sperling, Anne I. Wilson, Patrick C. Gajewski, Thomas F. Hubbell, Jeffrey A. Swartz, Melody A. |
author_sort | Briquez, Priscilla S. |
collection | PubMed |
description | Patients infected with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can experience life-threatening respiratory distress, blood pressure dysregulation and thrombosis. This is thought to be associated with an impaired activity of angiotensin-converting enzyme-2 (ACE-2), which is the main entry receptor of SARS-CoV-2 and which also tightly regulates blood pressure by converting the vasoconstrictive peptide angiotensin II (AngII) to a vasopressor peptide. Here, we show that a significant proportion of hospitalized COVID-19 patients developed autoantibodies against AngII, whose presence correlates with lower blood oxygenation, blood pressure dysregulation, and overall higher disease severity. Anti-AngII antibodies can develop upon specific immune reaction to the SARS-CoV-2 proteins Spike or RBD, to which they can cross-bind, suggesting some epitope mimicry between AngII and Spike/RBD. These results provide important insights on how an immune reaction against SARS-CoV-2 can impair blood pressure regulation. |
format | Online Article Text |
id | pubmed-8575143 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Cold Spring Harbor Laboratory |
record_format | MEDLINE/PubMed |
spelling | pubmed-85751432021-11-09 SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II Briquez, Priscilla S. Rouhani, Sherin J. Yu, Jovian Pyzer, Athalia R. Trujillo, Jonathan Dugan, Haley L. Stamper, Christopher T. Changrob, Siriruk Sperling, Anne I. Wilson, Patrick C. Gajewski, Thomas F. Hubbell, Jeffrey A. Swartz, Melody A. medRxiv Article Patients infected with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can experience life-threatening respiratory distress, blood pressure dysregulation and thrombosis. This is thought to be associated with an impaired activity of angiotensin-converting enzyme-2 (ACE-2), which is the main entry receptor of SARS-CoV-2 and which also tightly regulates blood pressure by converting the vasoconstrictive peptide angiotensin II (AngII) to a vasopressor peptide. Here, we show that a significant proportion of hospitalized COVID-19 patients developed autoantibodies against AngII, whose presence correlates with lower blood oxygenation, blood pressure dysregulation, and overall higher disease severity. Anti-AngII antibodies can develop upon specific immune reaction to the SARS-CoV-2 proteins Spike or RBD, to which they can cross-bind, suggesting some epitope mimicry between AngII and Spike/RBD. These results provide important insights on how an immune reaction against SARS-CoV-2 can impair blood pressure regulation. Cold Spring Harbor Laboratory 2021-11-02 /pmc/articles/PMC8575143/ /pubmed/34751272 http://dx.doi.org/10.1101/2021.11.02.21265789 Text en https://creativecommons.org/licenses/by-nc-nd/4.0/This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which allows reusers to copy and distribute the material in any medium or format in unadapted form only, for noncommercial purposes only, and only so long as attribution is given to the creator. |
spellingShingle | Article Briquez, Priscilla S. Rouhani, Sherin J. Yu, Jovian Pyzer, Athalia R. Trujillo, Jonathan Dugan, Haley L. Stamper, Christopher T. Changrob, Siriruk Sperling, Anne I. Wilson, Patrick C. Gajewski, Thomas F. Hubbell, Jeffrey A. Swartz, Melody A. SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II |
title | SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II |
title_full | SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II |
title_fullStr | SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II |
title_full_unstemmed | SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II |
title_short | SARS-CoV-2 infection induces cross-reactive autoantibodies against angiotensin II |
title_sort | sars-cov-2 infection induces cross-reactive autoantibodies against angiotensin ii |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8575143/ https://www.ncbi.nlm.nih.gov/pubmed/34751272 http://dx.doi.org/10.1101/2021.11.02.21265789 |
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