Document Type

Article

Publication Date

8-17-2022

Publication Title

Cell systems

Keywords

JGM, COVID-19, GWAS, Mendelian randomization, NK cell, gene discovery, genome-wide association study, machine learning, network analysis, rare variant analysis, single-cell multiomic profiling

JAX Source

Cell Syst . 2022 Aug 17;13(8):598-614.e6.

Volume

13

Issue

8

First Page

598

Last Page

614000000

PMID

35690068

DOI

10.1016/j.cels.2022.05.007

Grant

We acknowledge the Stanford Genetics Bioinformatics Service Center (GBSC) for providing computational infrastructure for this study. This study was sup- ported by the National Institutes of Health (1S10OD023452-01 to GBSC; CEGS 5P50HG00773504, 1P50HL083800, 1R01HL101388, 1R01-HL122939, S10OD025212, P30DK116074, and UM1HG009442 to M.P.S.) and the Wellcome Trust (216596/Z/19/Z to J.C.-K.). Figure 1 was created with BioRender.com. We thank the COVID-19 Host Genetics Initiative (https:// www.covid19hg.org/) for releasing the summary statistics data of GWAS and rare variant association study. We also thank GenOMICC (https://genomicc. org/) for sharing the GWAS summary statistics data to us.

Abstract

The determinants of severe COVID-19 in healthy adults are poorly understood, which limits the opportunity for early intervention. We present a multiomic analysis using machine learning to characterize the genomic basis of COVID-19 severity. We use single-cell multiome profiling of human lungs to link genetic signals to cell-type-specific functions. We discover >1,000 risk genes across 19 cell types, which account for 77% of the SNP-based heritability for severe disease. Genetic risk is particularly focused within natural killer (NK) cells and T cells, placing the dysfunction of these cells upstream of severe disease. Mendelian randomization and single-cell profiling of human NK cells support the role of NK cells and further localize genetic risk to CD56 NK cells, which are key cytokine producers during the innate immune response. Rare variant analysis confirms the enrichment of severe-disease-associated genetic variation within NK-cell risk genes. Our study provides insights into the pathogenesis of severe COVID-19 with potential therapeutic targets.

Comments

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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