Abstract

Coronavirus disease of 2019 (COVID-19) is the disease state caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for the current pandemic. SARS-CoV-2 infects cells via the membrane bound form of angiotensin converting enzyme 2 (ACE2). Aside from its role in viral entry, the role of ACE2 in the morbidity and mortality of severe COVID-19 is often overlooked. ACE2 functions as a member of the renin-angiotensin system (RAS) by cleaving the angiotensin II into angiotensin (1-7). Angiotensin II increases inflammation, thrombosis, and inflammation, whereas angiotensin (1-7) decreases these phenomena, making ACE2 an important balancing agent. ACE2 is downregulated in severe COVID-19 by both viral entry, which internalizes it, and the increased activity of “a disintegrin and metalloprotease 17” (ADAM17), which cleaves it off the membrane, delocalizing it. A meta-analysis was performed to demonstrate the striking resemblance between ACE2 downregulation and severe COVID-19. Sources were examined according to organ, type of ACE2 downregulation, and symptom. The downregulation of ACE2 exhibits similar symptoms in each organ for each pathology. RAS-based treatments of severe COVID-19 attempt to counter the downregulation of ACE2 prevalent in the disease. The most promising is human recombinant soluble ACE2 (hrsACE2; APN01), which both blocks viral entry and increases the functional ACE2 in the body. It is hoped that this study elucidates what is known and highlights understudied aspects of ACE2 and its role in COVID-19.

Semester/Year of Award

Spring 5-3-2021

Mentor

Oliver R. Oakley

Mentor Department Affiliation

Biological Sciences

Access Options

Open Access Thesis

Document Type

Bachelor Thesis

Degree Name

Honors Scholars

Degree Level

Bachelor's

Department

Biological Sciences

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