Author: William T Gibson; Daniel M Evans; Jianghong An; Steven JM Jones
Title: ACE 2 Coding Variants: A Potential X-linked Risk Factor for COVID-19 Disease Document date: 2020_4_14
ID: 05w8tv8x_21
Snippet: Applying the method of Schapira et al., 24 The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.04.05.026633 doi: bioRxiv preprint measures of environmental exposures, and typically identify tagging SNPs linked to loci with small 278 effect sizes. These methods, their attendant complexities, and the conservative genomewide thresholds 279 they require are justified by the fact that previous can.....
Document: Applying the method of Schapira et al., 24 The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.04.05.026633 doi: bioRxiv preprint measures of environmental exposures, and typically identify tagging SNPs linked to loci with small 278 effect sizes. These methods, their attendant complexities, and the conservative genomewide thresholds 279 they require are justified by the fact that previous candidate-gene studies had extremely high false-280 discovery rates, 33 largely due to the use of convenience samples that generated artefactual signals 281 owing to population stratification (i.e. the fact that SNP allele frequencies vary between ancestral 282 populations for historical reasons that are unrelated to heritable risk for disease). However, given the 283 truly staggering number of SARS-CoV-2 infections and the rapid progression from COVID-19 to death 284 (often within 14 days), such labour-intensive gene-agnostic methods are unlikely to yield clinically-285
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