作者
Athanasios Kousathanas, Erola Pairo-Castineira, Konrad Rawlik, Alex Stuckey, Christopher A Odhams, Susan Walker, Clark D Russell, Tomas Malinauskas, Yang Wu, Jonathan Millar, Xia Shen, Katherine S Elliott, Fiona Griffiths, Wilna Oosthuyzen, Kirstie Morrice, Sean Keating, Bo Wang, Daniel Rhodes, Lucija Klaric, Marie Zechner, Nick Parkinson, Afshan Siddiq, Peter Goddard, Sally Donovan, David Maslove, Alistair Nichol, Malcolm G Semple, Tala Zainy, Fiona Maleady-Crowe, Linda Todd, Shahla Salehi, Julian Knight, Greg Elgar, Georgia Chan, Prabhu Arumugam, Christine Patch, Augusto Rendon, David Bentley, Clare Kingsley, Jack A Kosmicki, Julie E Horowitz, Aris Baras, Goncalo R Abecasis, Manuel AR Ferreira, Anne Justice, Tooraj Mirshahi, Matthew Oetjens, Daniel J Rader, Marylyn D Ritchie, Anurag Verma, Tom A Fowler, Manu Shankar-Hari, Charlotte Summers, Charles Hinds, Peter Horby, Lowell Ling, Danny McAuley, Hugh Montgomery, Peter JM Openshaw, Paul Elliott, Timothy Walsh, Albert Tenesa, Angie Fawkes, Lee Murphy, Kathy Rowan, Chris P Ponting, Veronique Vitart, James F Wilson, Jian Yang, Andrew D Bretherick, Richard H Scott, Sara Clohisey Hendry, Loukas Moutsianas, Andy Law, Mark J Caulfield, J Kenneth Baillie
发表日期
2022/3/7
期刊
Nature
页码范围
1-10
出版商
Nature Publishing Group
简介
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization, – after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of …
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A Kousathanas, E Pairo-Castineira, K Rawlik… - Nature, 2022