The search for possible genetic clues behind the phenomenon of varying severity of COVID-19 has led researchers to several susceptible human genes which may play a role in the pathogenesis of the disease.
A study of over 2,600 twin volunteers conducted in 2020 in the UK found that genetics determined about 50% of COVID-19 symptoms.
Last August, researchers carried out a genome-wide association study (GWAS) among 2,173 COVID-19 patients with local control populations. One region they identified is the locus that encodes blood type. They found that blood group A had a significantly higher risk of infection, while blood group O had a protective effect.
However, some recent studies indicate that blood group O did not appear to be protective against severe COVID-19 illness and death compared with other blood groups.
Additional genes involved in antiviral immune responses and inflammation were identified in the samples of 2,200 patients with severe COVID-19 who were treated at over 200 intensive care units in the UK last year.
In this study, the authors identified eight genetic sequences that were more common in patients with the severe form of the infection. These sequences involved genes related to the inflammatory response that is triggered in the presence of a viral attack.
For example, the chr12q24.13 variant is linked to genes activating the antiviral response (OAS1, OAS2, OAS3); chr19p13.2 variant is close to the gene that encodes the enzyme tyrosine kinase 2 (TYK2); chr19p13.3 encodes for dipeptidyl peptidase 9 (DPP9) and chr21q22.1 variant for the IFNAR2 interferon receptor gene.
Five of the sequences were replicated in a meta-analysis of a similar number of hospitalised cases from the COVID-19 Host Genetics Initiative.