Abstract

Pathogenesis of COVID-19 has been linked to the Angiotensin system. Angiotensin-converting enzyme (ACE2) has been recognized as the specific receptor of the SARS-CoV-2 virus, serves as a cellular receptor for SARS-CoV-2, suggesting that a person's vulnerability to infection may be controlled by how much of the ACE2 gene is expressed. It is also possible that the severity of COVID-19 is related to the equilibrium between ACE1 and ACE2 activity, which has been linked to the etiology of respiratory disorders. This study aimed to investigate the association of ACE1 I/D polymorphism with the severity of Covid-19. The study looked at 113 people-(50 healthy controls, 63 people with Covid). Results for the ACE2 rs4240157 T > C polymorphism were obtained. Logistic regression was used to evaluate the distribution frequencies of variables across the study groups. The ACE1-CC*CT genotype (p = 0.049) and male gender (p0.001) were related to severe COVID-19. COVID-19 severity was found to be associated with the ACE2–CT genotype through multiple logistic regression under the co-dominant inheritance model: CC*CT Allele, 95% CI (0.0104 to 0.2954), Significance level, (0.0007) Odd Ratio (0.0556); CC*TT Allele, 95% CI (0.1854 to 6.1927), Significance level, (0.9386) Odd Ratio (1.0714); and CT*TT (19.2857). This was assuming the ACE2–CC*CT genotype was connected with covid-19 severity. However, the ACE2 polymorphism did not affect the development of illness. In conclusion, male gender, malignancy, and the ACE1 genotype were linked to a negative result of COVID-19. Our results indicated that ACE1-C/T might affect COVID-19 severity; however, this association was hypertensive status-specific. However, this finding needs to be confirmed in additional large samples.

Full Text
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