Subject(s)
COVID-19 , Vitamin D Deficiency , Humans , Vitamin D , Vitamin D Deficiency/complications , VitaminsSubject(s)
COVID-19 , Vitamin D Deficiency , Humans , SARS-CoV-2 , Vitamin D , Vitamin D Deficiency/genetics , Vitamin D-Binding Protein/geneticsSubject(s)
COVID-19 , Peptidyl-Dipeptidase A/genetics , COVID-19/mortality , Genotype , Humans , Polymorphism, Genetic , VaccinationABSTRACT
Coronavirus disease (COVID-19) is an infectious disease caused by a newly discovered coronavirus, severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). There is growing evidence that host genetics play an important role in COVID-19 severity. Based on current knowledge about the human protein machinery for SARS-CoV-2 entry, the host innate immune response, and virus-host interactions, the potential effects of human genetic polymorphisms, which may contribute to clinical differences in SARS-CoV-2 pathogenesis, may help to determine the individual risk for COVID-19 infection and outcome.
Subject(s)
COVID-19 , Humans , Polymorphism, Genetic , SARS-CoV-2/geneticsSubject(s)
COVID-19 , Vitamin D Deficiency , Humans , SARS-CoV-2 , Vitamin D , Vitamin D Deficiency/genetics , Vitamin D-Binding Protein/geneticsSubject(s)
COVID-19 , Vitamin D Deficiency , Humans , SARS-CoV-2 , Vitamin D , Vitamin D Deficiency/genetics , Vitamin D-Binding Protein/geneticsSubject(s)
ABO Blood-Group System , COVID-19 , Disease Susceptibility , Humans , Risk Factors , SARS-CoV-2Subject(s)
Biological Products , COVID-19 , Vitamin D Deficiency , Child , Humans , SARS-CoV-2 , Vitamin D , Vitamin D Deficiency/genetics , Vitamin D-Binding Protein/geneticsABSTRACT
The outbreak of the COVID-19 pandemic shows a marked geographical variation in its prevalence and mortality. The question arises if the host genetic variation may (partly) affect the prevalence and mortality of COVID-19. We postulated that the geographical variation of human polymorphisms might partly explain the variable prevalence of the infection. We investigated some candidate genes that have the potential to play a role in the immune defense against COVID-19: complement component 3 (C3), galactoside 2-alpha-L-fucosyltransferase 2 (FUT2), haptoglobin (Hp), vitamin D binding protein (DBP), human homeostatic iron regulator protein (HFE), cystic fibrosis transmembrane conductance regulator (CFTR), and angiotensin-converting enzyme 1 (ACE1). In a univariate approach, ACE1 D/I, C3, CFTR, and HFE polymorphisms correlated significantly with COVID-19 prevalence/mortality, whereas Hp and FUT2 polymorphism did not show any significant correlations. In a multivariate analysis, only ACE1 D/I and C3 polymorphisms were determinants for COVID-19 prevalence/mortality. The other polymorphisms (CFTR, DBP, FUT2, HFE, and Hp) did not correlate with COVID-19 prevalence/mortality. Whereas ACE1 D/I polymorphism shows functional links with ACE2 (which is the receptor for the virus) in COVID-19, C3 can act as a critical step in the virus-induced inflammation. Our findings plead against a bystander role of the polymorphisms as a marker for historical migrations, which comigrate with causal genes involved in COVID-19 infection. Further studies are required to assess the clinical outcome of COVID-19 in C3S and ACE1 D allele carriers and to study the role of C3 and ACE1 D/I polymorphisms in COVID-19 and their potential effects on treatment response.