The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
New insights into genetic susceptibility of COVID-19: an ACE2 and TMPRSS2 polymorphism analysis
Open accessAbstract
Background: Coronavirus Disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has now been confirmed worldwide. Yet, COVID-19 is strangely and tragically selective. Morbidity and mortality due to COVID19 rise dramatically with age and co-existing health conditions, including cancer and cardiovascular diseases. Human genetic factors may contribute to the extremely high transmissibility of SARS-CoV-2 and to the relentlessly progressive disease observed in a small but significant proportion of infected individuals, but these factors are largely unknown. Main body: In this study, we investigated genetic susceptibility to COVID-19 by examining DNA polymorphisms in ACE2 and TMPRSS2 (two key host factors of SARS-CoV-2) from ~ 81,000 human genomes. We found unique genetic susceptibility across different populations in ACE2 and TMPRSS2. Specifically, ACE2 polymorphisms were found to be associated with cardiovascular and pulmonary conditions by altering the angiotensinogen-ACE2 interactions, such as p.Arg514Gly in the African/African-American population. Unique but prevalent polymorphisms (including p.Val160Met (rs12329760), an expression quantitative trait locus (eQTL)) in TMPRSS2, offer potential explanations for differential genetic susceptibility to COVID-19 as well as for risk factors, including those with cancer and the high-risk group of male patients. We further discussed that polymorphisms in ACE2 or TMPRSS2 could guide effective treatments (i.e., hydroxychloroquine and camostat) for COVID-19. Conclusion: This study suggested that ACE2 or TMPRSS2 DNA polymorphisms were likely associated with genetic susceptibility of COVID-19, which calls for a human genetics initiative for fighting the COVID-19 pandemic.
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Hoffmann, M., Kleine-Weber, H., Schroeder, S., Krüger, N., Herrler, T., Erichsen, S., Schiergens, T. S., Herrler, G., Wu, N.-H., Nitsche, A., et al. (2020) · Cell · doi:10.1016/j.cell.2020.02.052 · Cited by 20,286
ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data
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An interactive web-based dashboard to track COVID-19 in real time
Dong, E., Du, H., & Gardner, L. (2020) · The Lancet Infectious Diseases · doi:10.1016/s1473-3099(20)30120-1 · Cited by 10,048
Analysis of protein-coding genetic variation in 60,706 humans
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The Genotype-Tissue Expression (GTEx) pilot analysis: Multitissue gene regulation in humans
The GTEx Consortium, Ardlie, K. G., Deluca, D. S., Segrè, A. V., Sullivan, T. J., Young, T. R., Gelfand, E. T., Trowbridge, C. A., Maller, J. B., Tukiainen, T., et al. (2015) · Science · doi:10.1126/science.1262110 · Cited by 5,062
Structural basis for the recognition of SARS-CoV-2 by full-length human ACE2
Yan, R., Zhang, Y., Li, Y., Xia, L., Guo, Y., & Zhou, Q. (2020) · Science · doi:10.1126/science.abb2762 · Cited by 5,040
Cardiovascular implications of fatal outcomes of patients with Coronavirus Disease 2019 (COVID-19)
Guo, T., Fan, Y., Chen, M., Wu, X., Zhang, L., He, T., Wang, H., Wan, J., Wang, X., & Lu, Z. (2020) · JAMA Cardiology · doi:10.1001/jamacardio.2020.1017 · Cited by 4,194
Epidemiology of COVID-19 Among Children in China
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Pharmacologic Treatments for Coronavirus Disease 2019 (COVID-19): A Review
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Artificial intelligence in COVID-19 drug repurposing
Zhou, Y., Wang, F., Tang, J., Nussinov, R., & Cheng, F. (2020) · The Lancet Digital Health · doi:10.1016/s2589-7500(20)30192-8 · Cited by 636
COVID-19 and Cardiovascular Disease: From Bench to Bedside
Chung, M. K., Zidar, D. A., Bristow, M. R., Cameron, S. J., Chan, T., Harding, C. V., Kwon, D. H., Singh, T., Tilton, J. C., Tsai, E. J., et al. (2021) · Circulation Research · doi:10.1161/circresaha.121.317997 · Cited by 373
Self-citationCOVID-19, immunothrombosis and venous thromboembolism: biological mechanisms
Loo, J., Spittle, D. A., & Newnham, M. (2021) · Thorax · doi:10.1136/thoraxjnl-2020-216243 · Cited by 341
Human ACE2 receptor polymorphisms and altered susceptibility to SARS-CoV-2
Suryamohan, K., Diwanji, D., Stawiski, E. W., Gupta, R., Miersch, S., Liu, J., Chen, C., Jiang, Y.-P., Fellouse, F. A., Sathirapongsasuti, J. F., et al. (2021) · Communications Biology · doi:10.1038/s42003-021-02030-3 · Cited by 299
APOE interacts with ACE2 inhibiting SARS-CoV-2 cellular entry and inflammation in COVID-19 patients
Zhang, H., Shao, L., Lin, Z., Long, Q.-X., Yuan, H., Cai, L., Jiang, G., Guo, X., Yang, R., Zhang, Z., et al. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01118-4 · Cited by 67
Metadata
- Authors
- Hou, Y., Zhao, J., Martin, W., Kallianpur, A., Chung, M. K., Jehi, L., Sharifi, N., Erzurum, S., Eng, C., & Cheng, F.
- Venue
- BMC Medicine
- Published
- 2020-07-15
- Volume
- 18
- Issue
- 1
- Pages
- 216-216
- ISSN
- 1741-7015 (ISSN-L)
- OpenAlex
- W3042860993
- Cited by
- 438
- References
- 28
- FWCI
- 11.44
- Type
- journal article
- Language
- en
- Open access
- gold
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- Hou, Y., Zhao, J., Martin, W., Kallianpur, A., Chung, M. K., Jehi, L., Sharifi, N., Erzurum, S., Eng, C., & Cheng, F. (2020). New insights into genetic susceptibility of COVID-19: an ACE2 and TMPRSS2 polymorphism analysis. BMC Medicine. https://doi.org/10.1186/s12916-020-01673-z
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