Genetic association analysis of SARS-CoV-2 infection in 455,838 UK Biobank participants
Kosmicki, J. A.; Horowitz, J. E.; Banerjee, N.; Lanche, R.; Marcketta, A.; Maxwell, E.; Bai, X.; Sun, D.; Backman, J.; Sharma, D.; O'Dushlaine, C.; Yadav, A.; Mansfield, A.; Li, A.; Mbatchou, J.; Watanabe, K.; Gurski, L.; McCarthy, S.; Locke, A.; Khalid, S.; Chazara, O.; Huang, Y.; Kvikstad, E.; Nadkar, A.; O'Neill, A.; Nioi, P.; Parker, M. M.; Petrovski, S.; Runz, H.; Szustakowski, J.; Wang, Q.; Jones, M.; Balasubramanian, S.; Salerno, W.; Shuldiner, A.; Marchini, J.; Overton, J.; Habegger, L.; Cantor, M.; Reid, J.; Baras, A.; Abecasis, G. R.; Ferreira, M. A.
10.1101/2020.10.28.20221804 medRxivShow abstract
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) causes coronavirus disease-19 (COVID-19), a respiratory illness that can result in hospitalization or death. We investigated associations between rare genetic variants and seven COVID-19 outcomes in 543,213 individuals, including 8,248 with COVID-19. After accounting for multiple testing, we did not identify any clear associations with rare variants either exome-wide or when specifically focusing on (i) 14 interferon pathway genes in which rare deleterious variants have been reported in severe COVID-19 patients; (ii) 167 genes located in COVID-19 GWAS risk loci; or (iii) 32 additional genes of immunologic relevance and/or therapeutic potential. Our analyses indicate there are no significant associations with rare protein-coding variants with detectable effect sizes at our current sample sizes. Analyses will be updated as additional data become available, with results publicly browsable at https://rgc-covid19.regeneron.com.
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