tetano
Editor, Senior Moderator
Sci Adv
. 2022 Oct 7;8(40):eabn3777.
doi: 10.1126/sciadv.abn3777. Epub 2022 Oct 7.
Severe COVID-19 induces autoantibodies against angiotensin II that correlate with blood pressure dysregulation and disease severity
Priscilla S Briquez[SUP] 1 2 [/SUP], Sherin J Rouhani[SUP] 3 [/SUP], Jovian Yu[SUP] 3 [/SUP], Athalia R Pyzer[SUP] 3 [/SUP], Jonathan Trujillo[SUP] 3 [/SUP], Haley L Dugan[SUP] 4 5 [/SUP], Christopher T Stamper[SUP] 4 5 6 [/SUP], Siriruk Changrob[SUP] 4 [/SUP], Anne I Sperling[SUP] 5 7 8 [/SUP], Patrick C Wilson[SUP] 4 5 [/SUP], Thomas F Gajewski[SUP] 3 5 9 10 [/SUP], Jeffrey A Hubbell[SUP] 1 5 10 [/SUP], Melody A Swartz[SUP] 1 5 9 10 [/SUP]
Affiliations
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.
. 2022 Oct 7;8(40):eabn3777.
doi: 10.1126/sciadv.abn3777. Epub 2022 Oct 7.
Severe COVID-19 induces autoantibodies against angiotensin II that correlate with blood pressure dysregulation and disease severity
Priscilla S Briquez[SUP] 1 2 [/SUP], Sherin J Rouhani[SUP] 3 [/SUP], Jovian Yu[SUP] 3 [/SUP], Athalia R Pyzer[SUP] 3 [/SUP], Jonathan Trujillo[SUP] 3 [/SUP], Haley L Dugan[SUP] 4 5 [/SUP], Christopher T Stamper[SUP] 4 5 6 [/SUP], Siriruk Changrob[SUP] 4 [/SUP], Anne I Sperling[SUP] 5 7 8 [/SUP], Patrick C Wilson[SUP] 4 5 [/SUP], Thomas F Gajewski[SUP] 3 5 9 10 [/SUP], Jeffrey A Hubbell[SUP] 1 5 10 [/SUP], Melody A Swartz[SUP] 1 5 9 10 [/SUP]
Affiliations
- PMID: 36206332
- DOI: 10.1126/sciadv.abn3777
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.