Detection the Genetic Polymorphisms of the Programmed Cell Death Gene PD1.3 G/A (rs11568821) in Coronavirus Disease Patients

Abstract

Abstract Background: Programmed cell death-1 protein (PD-1, Pcd1), a receptor from the CD28/CTLA-4 group, inhibits antigen receptor signaling by attracting protein tyrosine phosphatase in response to an interaction with any of the two ligands, PD-L1 or PD-L2. Human phenotypic variations can be attributed to both genetic and environmental influences. Objectives: Because SNPs (single nucleotide polymorphisms) are not absolute indicators of disease progression, in this work, the PD-1 gene polymorphism in coronavirus disease (COVID-19) patients was examined to assess the presence of SNPs in viral infections, in particular COVID-19 is the main goal of this investigation. Materials and Methods: Sixty confirmed COVID-19 patients were recruited to this study; 30 of them had severe COVID-19, whereas the other patients showed moderate sickness, who were admitted to the COVID-19 specialized ward in Salahuddin province, and all of them were over the age of 18 years. Also 30 healthy subjects were recruited for the purpose of the comparison. Blood was drawn from all the subjects for polymerase chain reaction (PCR) using the restriction fragment length (RFLP)-PCR for the assessment of the G/A SNP genotype of PD1.3 and ELISA test for the estimation of PD-1 and PD-L-1 serum level. Results: The examined PD-1 SNPs did not correlate with the incidence of COVID-19, according to a data analysis. Both the dominant and recessive models used in the research failed to detect a connection with the risk of COVID-19 severity. The PD1.3 genotypes frequency between the two groups did not show significant differences (P > 0.05). Only AG was substantially and mainly linked to COVID-19 susceptibility. This study compared the concentrations of immune check point inhibitors PD-1, PD-L-1 to find possible association with genotype frequency, and approved that PD-1 did not have any significant differences in the three groups of genotypes, whereas the difference was highly significant (0.048) in PDL-1 and AA genotype. Conclusion: Among all calculated haplotypes were unrelated to the disease’s prognosis (P > 0.05) concluded that the frequency of AA genotype in patients group decreed the expiation of PD-L-1, leads to immune inhibitions. Future research may clarify the relationship between some immune checkpoint molecule polymorphisms.