COVID-19 Research Paper Volume 12, Issue 20 pp 19880—19897
Single-cell expression profiles of ACE2 and TMPRSS2 reveals potential vertical transmission and fetus infection of SARS-CoV-2
- 1 Affiliated Cancer Hospital and Institute of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, Guangzhou, China
- 2 Joint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, Institute of Translational Medicine, School of Basic Medicine, Henan University, Kaifeng, China
- 3 Department of Clinical Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, China
- 4 Department of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
Received: April 16, 2020 Accepted: August 22, 2020 Published: October 26, 2020
https://doi.org/10.18632/aging.104015How to Cite
Copyright: © 2020 Lü et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Morbidity and mortality of coronavirus disease 2019 (COVID-19) is age-dependent. It remains unclear whether vertical severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) occurs during pregnancy and how such infection will affect fetal development. Here, we performed single-cell transcriptomic analysis of placenta and other tissues from fetuses in comparison with those from adults using public-available datasets. Our analysis revealed that a very small proportion of trophoblast cells expressed the Angiotensin I Converting Enzyme 2 (ACE2) gene, suggesting a low possibility of vertical transmission of SARS-CoV-2 from mother to fetus during pregnancy. We found that the fetal adrenal gland, heart, kidney and stomach were susceptible to SARS-CoV-2 infection, because these organs contained cell clusters that expressed high levels of the ACE2 gene. In particular, a higher proportion of ACE2-expressing cell clusters in the adrenal gland and kidney also expressed the Transmembrane Serine Protease 2 (TMPRSS2) gene compared with other organs. Surprisingly, ACE2-expressing type II alveolar (AT2) equivalent cells were absent in fetal lungs. This is in sharp contrast to adult lungs. As ACE2 expression is regulated by various conditions, including oxygen concentration, inflammation and smoking, caution is warranted to avoid triggering potential ACE2 expression in fetal and placental tissue.