PMC:7121452 / 9055-10652 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7121452","sourcedb":"PMC","sourceid":"7121452","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7121452","text":"SARS-CoV-2 appears not only to gain initial entry through ACE2 but also to subsequently down-regulate ACE2 expression such that the enzyme is unable to exert protective effects in organs. It has been postulated but unproven that unabated angiotensin II activity may be in part responsible for organ injury in Covid-19.43,44 After the initial engagement of SARS-CoV-2 spike protein, there is subsequent down-regulation of ACE2 abundance on cell surfaces.45 Continued viral infection and replication contribute to reduced membrane ACE2 expression, at least in vitro in cultured cells.46 Down-regulation of ACE2 activity in the lungs facilitates the initial neutrophil infiltration in response to bacterial endotoxin47 and may result in unopposed angiotensin II accumulation and local RAAS activation. Indeed, in experimental mouse models, exposure to SARS-CoV-1 spike protein induced acute lung injury, which is limited by RAAS blockade.45 Other mouse models have suggested that dysregulation of ACE2 may mediate acute lung injury that is secondary to virulent strains of influenza48,49 and respiratory syncytial virus.50 In a small study, patients with Covid-19 appeared to have elevated levels of plasma angiotensin II, which were in turn correlated with total viral load and degree of lung injury.44 Restoration of ACE2 through the administration of recombinant ACE2 appeared to reverse this devastating lung-injury process in preclinical models of other viral infections49,50 and safely reduced angiotensin II levels in a phase 2 trial evaluating acute respiratory distress syndrome in 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