Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes

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. Preprints 2020, 2020030356 (doi: 10.20944/preprints202003.0356.v1). Tanigawa, Y.; Rivas, M. Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes. Preprints 2020, 2020030356 (doi: 10.20944/preprints202003.0356.v1). Copy

Cite as: Tanigawa, Y.; Rivas, M. Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes. Preprints 2020, 2020030356 (doi: 10.20944/preprints202003.0356.v1). Tanigawa, Y.; Rivas, M. Initial Review and Analysis of COVID-19 Host Genetics and Associated Phenotypes. Preprints 2020, 2020030356 (doi: 10.20944/preprints202003.0356.v1). Copy CANCEL COPY CITATION DETAILS

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.

Supplementary and Associated Material

https://github.com/rivas-lab/covid19: Analysis scripts and notebooks https://tinyurl.com/abo-covid19: Publicly accessible Spreadsheet to share ABO blood group counts https://github.com/rivas-lab/covid19/tree/master/UKB_HLA_freq: HLA allelotype frequencies https://github.com/rivas-lab/covid19/tree/master/ABO: ABO blood group frequencies https://github.com/rivas-lab/covid19/tree/master/snpnet: Polygenic risk score (PRS) weights

Subject Areas

COVID-19; SARS-CoV-2; host genetics; genetics; polygenic risk score

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.

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