Genetic Susceptibility of Covid-19: A Systematic Review of Current Evidence Publisher Pubmed



Seyedalinaghi SA¹ ; Mehrtak M² ; Mohssenipour M¹ ; Mirzapour P¹ ; Barzegary A³ ; Habibi P¹ ; Moradmandbadie B⁴ ; Afsahi AM⁵ ; Karimi A⁶ ; Heydari M⁷ ; Mehraeen E⁷ ; Dadras O⁸ ; Sabatier JM⁹ ; Voltarelli F¹⁰
Source: European Journal of Medical Research Published:2021

Abstract

Introduction: While COVID-19 pandemic continues to spread worldwide, researchers have linked patterns of traits to poor disease outcomes. Risk factors for COVID-19 include asthma, elderly age, being pregnant, having any underlying diseases such as cardiovascular disease, diabetes, obesity, and experiencing lifelong systemic racism. Recently, connections to certain genes have also been found, although the susceptibility has not yet been established. We aimed to investigate the available evidence for the genetic susceptibility to COVID-19. Methods: This study was a systematic review of current evidence to investigate the genetic susceptibility of COVID-19. By systematic search and utilizing the keywords in the online databases including Scopus, PubMed, Web of Science, and Science Direct, we retrieved all the related papers and reports published in English from December 2019 to September 2020. Results: According to the findings, COVID-19 uses the angiotensin-converting enzyme 2 (ACE2) receptor for cell entry. Previous studies have shown that people with ACE2 polymorphism who have type 2 transmembrane serine proteases (TMPRSS2) are at high risk of SARS-CoV-2 infection. Also, two studies have shown that males are more likely to become infected with SARS-CoV-2 than females. Besides, research has also shown that patients possessing HLA-B*15:03 genotype may become immune to the infection. Conclusion: Combing through the genome, several genes related to immune system’s response were related to the severity and susceptibility to the COVID-19. In conclusion, a correlation was found between the ACE2 levels and the susceptibility to SARS-CoV-2 infection. © 2021, The Author(s).