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 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.
| Errataetall: |
UpdateIn: Sci Adv. 2022 Oct 7;8(40):eabn3777. - PMID 36206332 |
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| Medienart: |
E-Artikel |
| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - year:2021 |
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| Enthalten in: |
medRxiv : the preprint server for health sciences - (2021) vom: 02. Nov. |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Briquez, Priscilla S [VerfasserIn] |
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Date Revised 14.02.2024 published: Electronic UpdateIn: Sci Adv. 2022 Oct 7;8(40):eabn3777. - PMID 36206332 Citation Status PubMed-not-MEDLINE |
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| doi: |
10.1101/2021.11.02.21265789 |
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| PPN (Katalog-ID): |
NLM332892808 |
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| 520 | |a 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 | ||
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| 700 | 1 | |a Yu, Jovian |e verfasserin |4 aut | |
| 700 | 1 | |a Pyzer, Athalia R |e verfasserin |4 aut | |
| 700 | 1 | |a Trujillo, Jonathan |e verfasserin |4 aut | |
| 700 | 1 | |a Dugan, Haley L |e verfasserin |4 aut | |
| 700 | 1 | |a Stamper, Christopher T |e verfasserin |4 aut | |
| 700 | 1 | |a Changrob, Siriruk |e verfasserin |4 aut | |
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