Abstract

The rapid rise and global consequences of the novel coronavirus disease 19 (COVID-19) have again brought the focus of the scientific community on the possible host factors involved in patient response and outcome to exposure to the virus. The disease severity remains highly unpredictable, and individuals with none of the aforementioned risk factors may still develop severe COVID-19. It was shown that genotype-related factors like an ABO Blood Group affect COVID-19 severity, and the risk of infection with SARS-CoV-2 was higher for patients with blood type A and lower for patients with blood type O. Currently it is not clear which specific genes are associated with COVID-19 severity. The comparative analysis of COVID-19 and other viral infections allows us to predict that the variants within the interferon pathway genes may serve as markers of the magnitude of immune response to specific pathogens. In particular, various members of Class III interferons (lambda) are reviewed in detail.

Highlights

  • Coronavirus disease 2019 (COVID-19) is a rapidly emerging infectious disease caused by SARSCoV-2 virus, a member of the Coronaviridae family

  • In addition to findings reported from Italy/Spain (The Severe Covid-19 GWAS Group, 2020), a separate study comprising 3,199 hospitalized patients with COVID-19 and control individuals was released by the COVID-19 Host Genetics Initiative in which the region on chromosome 3 was the only major genetic risk factor for severe symptoms after SARS-CoV-2 infection and hospitalization at the genome-wide level (The COVID-19 Host Genetics Initiative, 2020)

  • In Caucasian populations, the CC genotype of rs12979860, which is associated with favourable hepatitis C virus (HCV) outcomes, is associated with spontaneous control of human immunodeficiency virus (HIV) viremia (Machmach et al, 2013)

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Summary

INTRODUCTION

Coronavirus disease 2019 (COVID-19) is a rapidly emerging infectious disease caused by SARSCoV-2 virus, a member of the Coronaviridae family. Studies attempting to connect variation in ACE2 and TMPRSS2 loci on the risks of contracting COVID-19 in any form, so far, have produced inconclusive results, ranging from single SNP associations uncovered in small cohorts (Latini et al, 2020) to the lack thereof. The latter, possibly, is due to the dual role of ACE2, which serves both as an entry into the wells and a lungprotective molecule (Dalan et al, 2020; Nagy et al, 2021). There remains continued interest in studying the ACE2 and TMPRSS2 genes as determinants of susceptibility to SARS-CoV-2

ABO Blood Group and Disease Severity
Other Loci
Tissue expression pattern
CONCLUSION
AUTHOR CONTRIBUTIONS
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