Entry of SARS-COV-2 into mammalian cells is mediated by angiotensin-converting enzyme 2 (ACE2). This binding and consequent ACE2 endocytosis have potential to disrupt blood stress regulation by interfering with ACE2-mediated cleavage of angiotensin II (AngII). Now, Swartz and colleagues recommend that SARS-CoV-2 an infection may additionally dysregulate vascular stress in sufferers with extreme COVID-19 by selling the formation of anti-AngII autoantibodies.
Credit score: Springer Nature Restricted
The researchers detected anti-ACE2 antibodies in serum from hospitalized sufferers with COVID-19, and the antibody ranges correlated strongly with blood stress dysregulation and illness severity (based mostly on blood oxygenation ranges). Mouse monoclonal anti-AngII antibodies cross-reacted with recombinant SARS-CoV-2 spike protein, indicating that epitope mimicry may contribute to the technology of autoantibodies in contaminated people. In vitro, monoclonal anti-ACE2 antibodies interfered with binding of AngII to AngII receptor sort 1, suggesting antagonism of AngII operate.
