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The causative virus for the current COVID-19 pandemic, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) employs angiotensin converting enzyme-2 (ACE2) as a co-receptor for viral entry into host cells Since ACE2 is also an important constituent of the renin-angiotensin-system (RAS), it has been argued that blockers of the RAS such as ACE-inhibitors (ACEi) or angiotensin-receptor blockers (ARBs) might modify ACE2 expression in host cells and thereby alter virus susceptibility beyond hypothetical effects of RAS blockers on the clinical course of viral disease Here, we provide a detailed overview of both the classical RAS axis and the so-called alternative RAS axis that includes ACE2 and its end-product angiotensin-1-7 and how they might theoretically affect viral susceptibility and disease progression From the models outlined it becomes clear that any clinical inferences such as to halt or convert established RAS-blocking regimens in patients with heart failure and chronic kidney disease is rather preemptive, thereby enforcing current recommendations from several national and international societies
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Angiotensin-Blockade and COVID-19: Hypotheses and clinical implications
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