Version 1
: Received: 4 March 2020 / Approved: 5 March 2020 / Online: 5 March 2020 (03:15:43 CET)
How to cite:
Wang, J.; Luo, Q.; Chen, R.; Chen, T.; Li, J. Susceptibility Analysis of COVID-19 in Smokers Based on ACE2. Preprints2020, 2020030078. https://doi.org/10.20944/preprints202003.0078.v1
Wang, J.; Luo, Q.; Chen, R.; Chen, T.; Li, J. Susceptibility Analysis of COVID-19 in Smokers Based on ACE2. Preprints 2020, 2020030078. https://doi.org/10.20944/preprints202003.0078.v1
Wang, J.; Luo, Q.; Chen, R.; Chen, T.; Li, J. Susceptibility Analysis of COVID-19 in Smokers Based on ACE2. Preprints2020, 2020030078. https://doi.org/10.20944/preprints202003.0078.v1
APA Style
Wang, J., Luo, Q., Chen, R., Chen, T., & Li, J. (2020). Susceptibility Analysis of COVID-19 in Smokers Based on ACE2. Preprints. https://doi.org/10.20944/preprints202003.0078.v1
Chicago/Turabian Style
Wang, J., Tao Chen and Jianxiang Li. 2020 "Susceptibility Analysis of COVID-19 in Smokers Based on ACE2" Preprints. https://doi.org/10.20944/preprints202003.0078.v1
Abstract
Background: Cigarette smoking (CS) is a global public health problem and a high-risk factor for various diseases. In December 2019, a novel coronavirus (HCoV-19) was identified in Wuhan, China. Because ACE2 has been identified as a receptor for HCoV-19, we hypothesize that CS affects the expression pattern of ACE2 in respiratory tract, causing differences in susceptibility to the virus. Methods: Three datasets (GSE994, GSE17913, and GSE18344), were downloaded from the Gene Expression Omnibus (GEO) database. Correlation and enrichment analysis were used to evaluate the function of ACE2. Also, the different expression of ACE2 in different groups of three datasets were analyzed. Results: Genes associated with ACE2 were enriched in important biological processes such as viral processes and immune response. Elevated ACE2 were found in intrapulmonary airways (GSE994) and oral epithelial cells (GSE17913) of smokers but not those of non-smokers or former smokers. Significant dose- and time-dependent relationships between CS and ACE2 expression were observed in mouse lung tissues, and long periods without smoking were found to significantly reduce ACE2 expression. Conclusions: Both human and rat data confirmed that CS could induce increased ACE2 in the respiratory tract, indicating that smokers have a higher susceptibility to HCoV-19.
Keywords
cigarette smoke; ACE2; HCoV-19; susceptibility
Subject
Biology and Life Sciences, Behavioral Sciences
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received:
25 March 2020
Commenter:
Dr Paolo Milan
The commenter has declared there is no conflict of interests.
Comment:
A Question
ACE2 has a dual action in the lung, it is CoV2 coronavirus receptor but it is also a protective factor for lung. Someone hypothesized that CoV2 virus may give downregulation of ace2, therefore smoking could absurdly have a protective role by increasing the expression of ace2 ? Thank'S
Commenter: Dr Paolo Milan
The commenter has declared there is no conflict of interests.
A Question
ACE2 has a dual action in the lung, it is CoV2 coronavirus receptor but it is also a protective factor for lung. Someone hypothesized that CoV2 virus may give downregulation of ace2, therefore smoking could absurdly have a protective role by increasing the expression of ace2 ? Thank'S