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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 t...

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Detalles Bibliográficos
Autores principales: 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.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8575143/
https://www.ncbi.nlm.nih.gov/pubmed/34751272
http://dx.doi.org/10.1101/2021.11.02.21265789
Descripción
Sumario: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.