Abstract
Coronavirus disease (COVID-19) presents a broad spectrum of clinical manifestations ranging from an asymptomatic to a severe clinical course. The host genetic background influence on the susceptibility and outcome of multiples infectious diseases has been previously reported. Herein, we aimed to describe relevant identified genetic variants and those potentially related to the inter-individual variability of COVID-19 susceptibility and/or severity considering the physiopathological pathway of the disease The HLA-A*25:01, -B*15:27, -B*46:01, -C*01:02, and -C*07:29 alleles have been associated with COVID-19 susceptibility; while HLA-A*02:02, -B*15:03, and -C*12:03 have been identified as low-risk alleles. Variants in cytokine genes such as IL1B, IL1R1, IL1RN, IL6, IL17A, FCGR2A, and TNF could be related to disease susceptibility and cytokine storm, and/or COVID-19 complications (e.g., venous thrombosis). Several variants in ACE2 and TMPRSS2 affecting the expression of the receptors related to COVID-19 have been associated with the disease susceptibility and risk factors. Finally, two GWAS have identified the loci 3p21.31 (LZTFL1, SLC6A20, CCR9, FYCO1, CXCR6, and XCR1) and 9q34.2 (ABO) with COVID-19 severity. Heterogeneous results in the association of genetic variants with COVID-19 susceptibility and severity were observed. The mechanism of identified risk-genes and studies in different populations are still warranted.
Highlights
The Coronavirus Disease 2019 (COVID-19) is a severe respiratory and systemic disease caused by the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)
Myocardial injury is strongly associated with death and severe cases of the COVID-19 [9, 11], and it has been explained by the presence of AngiotensinConverting Enzyme 2 (ACE2) in myocardial cells and the cytokine storm produced after the SARS-CoV-2 infection [12]
The involvement of Mannose-Binding Lectin (MBL) and MBL-associated serine protease (MASP)-1/3 in coagulation has been reported, and its deficiency has been considered as a risk factor for Disseminated Intravascular Coagulation (DIC) during sepsis complication; genetic variants producing a decrease of these proteins or their activity could be positively related with coagulopathies secondary to COVID-19 [99]
Summary
The Coronavirus Disease 2019 (COVID-19) is a severe respiratory and systemic disease caused by the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Myocardial injury (including acute coronary syndrome, myocarditis, heart failure, hypotension, shock, and sepsis) is strongly associated with death and severe cases of the COVID-19 [9, 11], and it has been explained by the presence of AngiotensinConverting Enzyme 2 (ACE2) in myocardial cells and the cytokine storm produced after the SARS-CoV-2 infection [12]. Given the broad spectrum of COVID-19 clinical course and complications, identifying risk factors that could predict the disease’s severity would improve the infected patients’ outcome In this sense, older age, smoking, hypertension, diabetes mellitus, cardiac disease, chronic lung disease, and cancer have been associated with COVID-19 severity and death [3, 14]. Information was analyzed and summarized; the analysis and conclusions of those results are reported in the present review
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