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SARS-CoV-2, ACE2 expression, and systemic organ invasion
Physiological Genomics  (IF3.107),  Pub Date : 2020-12-04, DOI: 10.1152/physiolgenomics.00087.2020
Usman M Ashraf, Ahmed A Abokor, Jonnelle M. Edwards, Emily W. Waigi, Rachel S. Royfman, Syed Abdul-Moiz Hasan, Kathryn B Smedlund, Ana Maria Gregio Hardy, Ritu Chakravarti, Lauren G. Koch

A novel coronavirus disease, COVID-19, has created a global pandemic in 2020, posing an enormous challenge to healthcare systems and affected communities. COVID-19 is caused by Severe Acute Respiratory Syndrome (SARS)-CoronaVirus-2 (CoV-2) that manifests as bronchitis, pneumonia, or a severe respiratory illness. SARS-CoV-2 infects human cells via binding a "spike" protein on its surface to angiotensin-converting enzyme 2 (ACE2) within the host. ACE2 is crucial for maintaining tissue homeostasis and negatively regulates the renin-angiotensin-aldosterone system (RAAS) in the humans. The RAAS is paramount for normal function in multiple organ systems including the lungs, heart, kidney, and vasculature. Given that SARS-CoV-2 internalizes via ACE2, the resultant disruption in ACE2 expression can lead to altered tissue function and exacerbate chronic diseases. The widespread distribution and expression of ACE2 across multiple organs is critical to our understanding of the varied clinical outcomes of COVID-19. This perspective review based on the current literature was prompted to show how disruption of ACE2 by SARS-CoV-2 can affect different organ systems.