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Severe COVID-19 induces autoantibodies against angiotensin II that correlate with blood pressure dysregulation and disease severity

Briquez, PS (author)
Rouhani, SJ (author)
Yu, J (author)
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Pyzer, AR (author)
Trujillo, J (author)
Dugan, HL (author)
Stamper, CT (author)
Karolinska Institutet
Changrob, S (author)
Sperling, AI (author)
Wilson, PC (author)
Gajewski, TF (author)
Hubbell, JA (author)
Swartz, MA (author)
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 (creator_code:org_t)
American Association for the Advancement of Science (AAAS), 2022
2022
English.
In: Science advances. - : American Association for the Advancement of Science (AAAS). - 2375-2548. ; 8:40, s. eabn3777-
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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 (ACE2), 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 patients with COVID-19 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 receptor-binding domain (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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