Biological Sciences Division
Published October 7, 2022 | Version v1
Journal article Open

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

Creators

  • 1. University of Chicago

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 (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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Additional details

Identifiers

DOI
10.1126/sciadv.abn3777
Other
oai:uchicago.tind.io:4996

Funding

Chicago Immunoengineering Innovation Center
Chicago Biomedical Consortium
University of Chicago's "Big Ideas Generator" for COVID research
T32 CA009566
National Institutes of Health
R01 AI125644

UChicago Information

Division(s)
Biological Sciences Division, Pritzker School of Molecular Engineering
Department(s)
Ben May Department for Cancer Research, Cancer Biology, Immunology, Medicine