Abstract

COVID-19 exhibits a wide range of phenotypic manifestations, from asymptomatic to severe phenotypes with fatal complications. The exis-tence of risk factors cannot entirely explain the variance in the phenotypic vari-ability of COVID-19. Genome-wide association analyses have identified target human genes related to virus transmission and the clinical phenotype observed in COVID-19 patients. Genetic variants on the OAS1 gene have been associ-ated with innate immune processes (entry phase and viral replication in host cells). The A or G alleles of rs10774671 in OAS1 encode isoforms with different antiviral activities. One hundred COVID-19 patients were genotyped for the rs10774671 using RFLP-PCR (severe form, n = 43; asymptomatic-mild, n = 57). The susceptibility of the two groups to the severe phenotype of COVID-19 was compared. The allele frequency for A was 0.8. The genotypic frequencies for AA and GG homozygotes were 0.62 and 0.02, respectively. A Hardy-Weinberg equilibrium deviation was found in both groups. No statistically significant as-sociations were found in genetic models adjusted for sex (for the additive model OR = 1.18, 95% CI = (0.53-2.61), p = 0.69). A relatively recent mix of different ethnic groups and sample size may influence these findings.

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