The human genetic epidemiology of COVID-19

In this article, Niemi, Daly and Ganna discuss how large-scale genomics studies are providing a rapidly maturing understanding of the influence of host genetics on coronavirus disease 2019 (COVID-19) susceptibility and severity. They also describe the implications for identifying causal mechanisms of pathology and potential therapeutic opportunities. Human genetics can inform the biology and epidemiology of coronavirus disease 2019 (COVID-19) by pinpointing causal mechanisms that explain why some individuals become more severely affected by the disease upon infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. Large-scale genetic association studies, encompassing both rare and common genetic variants, have used different study designs and multiple disease phenotype definitions to identify several genomic regions associated with COVID-19. Along with a multitude of follow-up studies, these findings have increased our understanding of disease aetiology and provided routes for management of COVID-19. Important emergent opportunities include the clinical translatability of genetic risk prediction, the repurposing of existing drugs, exploration of variable host effects of different viral strains, study of inter-individual variability in vaccination response and understanding the long-term consequences of SARS-CoV-2 infection. Beyond the current pandemic, these transferrable opportunities are likely to affect the study of many infectious diseases.

Automated summary

In this article, the authors discuss how large-scale genomics studies are helping us to better understand the impact of host genetics on COVID-19 susceptibility and severity. These studies have identified genomic regions associated with the disease and provided insights into its pathology and potential therapeutic opportunities. The findings have implications for genetic risk prediction, drug repurposing, and understanding the long-term consequences of SARS-CoV-2 infection.