Background Mannose-binding lectin (MBL) is a member of innate immunity and acts with MASP (MBL-associated serine protease) to activate the lectin pathway of the complement system. MBL gene polymorphisms are associated with susceptibility to infectious diseases. This study investigated whether MBL2 genotype, serum MBL levels, and serum MASP-2 levels affect the course of SARS-CoV-2 infection. Methods and results Pediatric patients diagnosed with COVID-19 by positive real-time polymerase chain reaction (PCR) were included in the study. Single nucleotide polymorphisms in the promoter and exon 1 in the MBL2 gene (rs11003125, rs7096206, rs1800450, rs1800451, rs5030737) were identified by a PCR and restriction fragment length polymorphisms analysis. Serum MBL and MASP-2 levels were measured by ELISA. COVID-19 patients were divided into asymptomatic and symptomatic. Variables were compared between these two groups. A total of 100 children were included in the study. The mean age of the patients was 130 ± 67.2 months. Of the patients, 68 (68%) were symptomatic, and 32 (32%) were asymptomatic. The polymorphisms in the − 221nt and − 550nt promoter regions did not differ between groups (p > 0.05). All codon 52 and codon 57 genotypes were determined as wild-type AA. AB genotypes were found 45.6% in symptomatic patients while 23.5% in asymptomatics. Moreover, BB genotype was detected 9.4% in symptomatic and 6.3% in asymptomatic patients (p < 0.001). B allele was more frequent in symptomatic patients (46.3%) compared to asymptomatic patients (10.9%). (p < 0.001). Serum MBL and MASP-2 levels did not differ statistically between the groups (p = 0.295, p = 0.073). Conclusion These findings suggest that codon 54 polymorphism in the MBL2 gene exon-1 region can be associated with the symptomatic course of COVID-19.

Aim: The coronavirus disease 2019 (COVID-19) was caused by severe acute respiratory syndrome 2 virus (SARS-CoV-2), has spread globally. Gender and age have been established as risk factors for severe COVID-19. However, these factors do not fully explain the effects on disease risk. According to researchers, single nucleotide polymorphisms (SNPs) on multiple genes could affect the severity of COVID-19. The progression of viral diseases depends on the characteristics of the patient's innate immunity. The effectiveness of the innate immune system depends on the patient's genetic factors, including SNPs in the TLR, CCR5, and RIG-I genes. In this study, we researched the association of allele and genotype frequency in SNPs of COVID-19 patients with age and gender. Materials and Methods: In our study, 200 patients with moderate COVID-19 were included. Single nucleotide polymorphisms (SNP) of TLR3 (rs3775291, rs3775290, rs5743305), TLR7 (rs179008), TLR8 (rs3764880), RIG-I (rs12006123), and CCR5 (rs1799987) were studied. SNPs were determined by restriction fragment length polymerase chain reaction (RFLP-PCR) methods. Results: In the COVID-19 patients, we examined the patients were evaluated in terms of allele and genotype frequencies and the association between some parameters like age, and gender. In our results, TLR3 rs5743305 AA genotype frequency (p=0.03) and TLR7 rs179008 AA genotype frequency (p=0.03) were found to be significant in terms of age and gender. Conclusions: These SNP data is assessed against disease risk to plan personalized pharmacological therapy for COVID-19 patients.The findings from this study will be useful for genome-wide association studies (GWAS).

Objective: After kidney transplantation, CD8+ T cells can infiltrate the kidney and cause necrosis, tubulitis, and even transplant rejection. For this reason, control of the T cell response is very important, and T cell immunoglobulin and mucin domain 3 (TIM-3) and programmed death 1 (PD-1) molecules play a role in regulating the T cell response. It is thought that the levels of TIM-3 and PD-1 expressions may be guiding in determining the clinical course after transplantation. This study aimed to determine the relationship between the mRNA levels of PD-1 and TIM-3 genes in peripheral blood samples taken from kidney transplant patients and the clinical conditions of the patients. Material and Method: 60 peripheral blood samples were collected from 30 kidney transplant patients, both pre-transplantation (pre-tx) and post-transplantation (post-tx). CD8+ T cells were separated from other lymphocytes by magnetic cell separation system (MACS) and their purity was determined by flow cytometry. Then, RNA was isolated and after cDNA conversion, the expressions of PD-1 and TIM-3 genes were determined by real-time polymerase chain reaction. Results: While it was determined that the TIM-3 gene expression level increased in patients with acute tubular necrosis, antibody-mediated rejection and cell-mediated rejection findings (p