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Genetic Polymorphisms in the Host and COVID-19 Infection
Joris R Delanghe1,2, Marc L De Buyzere3, Marijn M Speeckaert3,4
1Department of Diagnostic Sciences, Ghent University, Ghent, Belgium. joris.delanghe@ugent.be.
Advances in Experimental Medicine and Biology
|May 11, 2021
Summary
Host genetic variations, specifically angiotensin-converting enzyme 1 (ACE1) D/I and complement component 3 (C3) polymorphisms, significantly influence COVID-19 prevalence and mortality. These genetic factors may play a direct role in disease severity and inflammation.
Area of Science:
- Genetics
- Immunology
- Epidemiology
Background:
- COVID-19 pandemic exhibits significant geographical variations in prevalence and mortality.
- Host genetic factors are hypothesized to contribute to these observed geographical disparities.
Purpose of the Study:
- To investigate the association between specific human gene polymorphisms and COVID-19 prevalence and mortality.
- To identify genetic determinants of COVID-19 susceptibility and severity.
Main Methods:
- Examined polymorphisms in candidate immune defense genes: C3, FUT2, Hp, DBP, HFE, CFTR, and ACE1.
- Utilized univariate and multivariate analyses to assess correlations with COVID-19 prevalence/mortality.
Main Results:
- Univariate analysis revealed significant correlations for ACE1 D/I, C3, CFTR, and HFE polymorphisms.
- Multivariate analysis identified ACE1 D/I and C3 polymorphisms as key determinants of COVID-19 prevalence/mortality.
- CFTR, DBP, FUT2, HFE, and Hp polymorphisms showed no significant correlation in multivariate analysis.
Conclusions:
- ACE1 D/I and C3 polymorphisms are significant determinants of COVID-19 prevalence and mortality.
- Findings suggest a direct role for these polymorphisms in COVID-19 pathogenesis, rather than as markers of migration.
- Further research is needed to understand the clinical implications for carriers and potential treatment effects.
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