Abstract
The SARS-CoV-2 virus, which causes COVID-19, has been associated globally with substantial morbidity and mortality. Numerous reports over the past year have described the clinical and immunological profiles of COVID-19 patients, and while some trends have emerged for risk stratification, they do not provide a complete picture. Therefore, efforts are ongoing to identify genetic susceptibility factors of severe disease. In this issue of the JCI, Povysil et al. performed a large, multiple-country study, sequencing genomes from patients with mild and severe COVID-19, along with population controls. Contrary to previous reports, the authors observed no enrichment of predicted loss-of-function variants in genes in the type I interferon pathway, which might predispose to severe disease. These studies suggest that more evidence is needed to substantiate the hypothesis for a genetic immune predisposition to severe COVID-19, and highlights the importance of considering experimental design when implicating a monogenic basis for severe disease.
【초록키워드】 COVID-19, severe COVID-19, Sequencing, Genome, Genetic, variant, SARS-CoV-2 virus, immune, type I interferon, risk stratification, Patient, pathway, Mild, genetic susceptibility, morbidity and mortality, COVID-19 patients, Evidence, Hypothesis, severe disease, Factor, immunological profile, effort, loss-of-function, predisposition, experimental design, Complete, controls, highlight, described, predicted, identify, performed, cause, Numerous, 【제목키워드】 Immunity, susceptibility, monogenic inborn error,