Journal
GENOME BIOLOGY
Volume 22, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s13059-021-02454-4
Keywords
COVID-19; SARS-CoV-2; GWAS; eQTL; CRISPR
Funding
- NIH/NHLBI [R01HL142028]
- American Heart Association [20POST35220040]
- NIH/NIMH [R01MH106842]
- NIH [R01AI123155]
- Marc Haas Foundation
- National Institutes of Health
- DARPA's PREPARE Program [HR0011-202-0040]
- NYU startup fund
- NYGC startup fund
- NIH/NHGRI [DP2HG010099, UM1HG008901]
- NIH/NCI [R01CA218668]
- DARPA [D18AP00053]
- Sidney Kimmel Foundation
- Brain and Behavior Foundation
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The study identifies SLC6A20 and CXCR6 as potential causal genes that modulate COVID-19 risk by integrating genome-scale CRISPR loss-of-function screens and eQTLs in diverse cell types and tissues. This integrative approach bridges the gap between correlational and causal studies in human biology.
To date, the locus with the most robust human genetic association to COVID-19 severity is 3p21.31. Here, we integrate genome-scale CRISPR loss-of-function screens and eQTLs in diverse cell types and tissues to pinpoint genes underlying COVID-19 risk. Our findings identify SLC6A20 and CXCR6 as putative causal genes that modulate COVID-19 risk and highlight the usefulness of this integrative approach to bridge the divide between correlational and causal studies of human biology.
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