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Severe COVID-19 induces autoantibodies against angiotensin II that correlate with blood pressure dysregulation and disease severity.
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.
  • Briquez PS; Pritzker School for Molecular Engineering, University of Chicago, Chicago, IL, USA.
  • Rouhani SJ; Department of General and Visceral Surgery, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg 79106, Germany.
  • Yu J; Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL, USA.
  • Pyzer AR; Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL, USA.
  • Trujillo J; Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL, USA.
  • Dugan HL; Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL, USA.
  • Stamper CT; Department of Medicine, Section of Rheumatology, University of Chicago, Chicago, IL, USA.
  • Changrob S; Committee on Immunology, University of Chicago, Chicago, IL, USA.
  • Sperling AI; Department of Medicine, Section of Rheumatology, University of Chicago, Chicago, IL, USA.
  • Wilson PC; Committee on Immunology, University of Chicago, Chicago, IL, USA.
  • Gajewski TF; Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
  • Hubbell JA; Department of Medicine, Section of Rheumatology, University of Chicago, Chicago, IL, USA.
  • Swartz MA; Committee on Immunology, University of Chicago, Chicago, IL, USA.
Sci Adv ; 8(40): eabn3777, 2022 10 07.
Article in English | MEDLINE | ID: covidwho-2063966
ABSTRACT
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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Full text: Available Collection: International databases Database: MEDLINE Main subject: Angiotensin-Converting Enzyme 2 / COVID-19 Type of study: Prognostic study / Randomized controlled trials Limits: Humans Language: English Journal: Sci Adv Year: 2022 Document Type: Article Affiliation country: Sciadv.abn3777

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Angiotensin-Converting Enzyme 2 / COVID-19 Type of study: Prognostic study / Randomized controlled trials Limits: Humans Language: English Journal: Sci Adv Year: 2022 Document Type: Article Affiliation country: Sciadv.abn3777