Version 1
: Received: 23 March 2020 / Approved: 24 March 2020 / Online: 24 March 2020 (08:36:20 CET)
How to cite:
Tanigawa, Y.; Rivas, M. Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes. Preprints2020, 2020030356. https://doi.org/10.20944/preprints202003.0356.v1
Tanigawa, Y.; Rivas, M. Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes. Preprints 2020, 2020030356. https://doi.org/10.20944/preprints202003.0356.v1
Tanigawa, Y.; Rivas, M. Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes. Preprints2020, 2020030356. https://doi.org/10.20944/preprints202003.0356.v1
APA Style
Tanigawa, Y., & Rivas, M. (2020). Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes. Preprints. https://doi.org/10.20944/preprints202003.0356.v1
Chicago/Turabian Style
Tanigawa, Y. and Manuel Rivas. 2020 "Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes" Preprints. https://doi.org/10.20944/preprints202003.0356.v1
Abstract
The global pandemic of COVID-19 accounts for more than 14,000 deaths worldwide. However, little is known about the host genetics interaction with infection and COVID-19 progression. To better understand the role of host genetics, we review the current literature, aggregate readily available genetic resources, and provide some updated analysis relevant to COVID-19 and associated phenotypes. Using the unrelated individuals in UK Biobank (total n = 337,579 across 5 populations), we aggregate human leukocyte antigen and ABO blood type frequencies. We find significant and consistent risk reduction of blood group O reported in Zhao et al. and encourage broad sharing of ABO blood type frequencies that are readily accessible across COVID-19 with mild, moderate, and severe/critical symptoms for robust inferences at https://tinyurl.com/abo-covid19. In addition, we generate polygenic risk scores (PRSs) weights for 29 blood measurements, including clinically relevant haematological measurements for COVID-19, such as lymphocyte count and percentage. Focusing on the 8 most COVID-19 clinically relevant blood measurements, we performed PRS-PheWAS analysis across 44 disease antigen measurements (n = 6,643 unrelated individuals in White British group), infectious diseases and acute respiratory infections (n = 20,928 cases and 349,000 controls across 3 population groups) and deaths (n = 1,846 cases and 368,082 controls), recorded in hospital inpatient record and death registry data, respectively, in UK Biobank, and find host genetic PRS associations with disease risk. Taken together, we anticipate these resources (https://github.com/rivas-lab/covid19) will aid in improving our understanding of host genetic risk factors playing a role in SARS-CoV-2 infection and COVID-19 disease severity.
Biology and Life Sciences, Biochemistry and Molecular Biology
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:
10 April 2020
Commenter:
Stéphane Mazieres
The commenter has declared there is no conflict of interests.
Comment:
Dear,
I'm surprised how ABO phenotypes could be accurately inferred from these 3 snp.
One is correct (Leu266Met) but the 2 others are intronic and not responsible of the main ABO phenotypes according to the blood group nomenclature (see ISBT). Then the phenotypes are deduced from these 3 snp, 2 of which are false, when in fact, it takes 5.
Please consider the works of Yamamoto et al. 1990 that proved the causality.
Commenter:
The commenter has declared there is no conflict of interests.
https://biobankengine.shinyapps.io/hla-map/
Commenter:
The commenter has declared there is no conflict of interests.
https://github.com/rivas-lab/covid19/tree/master/HLA
Commenter: Stéphane Mazieres
The commenter has declared there is no conflict of interests.
I'm surprised how ABO phenotypes could be accurately inferred from these 3 snp.
One is correct (Leu266Met) but the 2 others are intronic and not responsible of the main ABO phenotypes according to the blood group nomenclature (see ISBT). Then the phenotypes are deduced from these 3 snp, 2 of which are false, when in fact, it takes 5.
Please consider the works of Yamamoto et al. 1990 that proved the causality.
Best regards,