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. 2020 Sep 22;5(1):15. doi: 10.1186/s41231-020-00067-w

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — The effect of ACE2 expression levels on COVID-19 disease and severity. Age, genetics, and different comorbidities affect the pre-infection ACE2 expression levels in a subset of individuals (left), rendering them susceptible to severe forms of disease. During infection (right), upon interaction of SARS-CoV-2 S protein with ACE2 and TMPRSS2, ACE2 levels are downregulated. Those individuals with low pre-infection ACE2 levels reach a threshold critical value corresponding to the onset of severe symptomathologies due to RAAS imbalance