ABSTRACT
Macrophage activation syndrome (MAS) is one of the main causes of morbidity and mortality in patients with coronavirus disease 2019 (COVID-19). This study aimed to investigate the relationship between the pentraxin 3 (PTX3) gene polymorphisms rs2305619 (281A/G) and rs1840680 (1449A/G) and the development of MAS in patients with COVID-19. The study included a total of 94 patients aged 18-45 who were diagnosed as having COVID-19 between June and December 2020. PTX3 281A/G and 1449A/G polymorphism frequencies were evaluated. PTX3 281A/G allele and genotype frequencies did not deviate from Hardy-Weinberg (HW) equilibrium in the MAS or non-MAS group (χ2 : 0.049, df: 2, p = 0.976, χ2 : 0.430, df: 2, p = 0.806). PTX3 1449A/G allele and genotype frequencies deviated significantly from HW equilibrium in the non-MAS group (χ2 : 6.794, df: 2, p = 0.033) but not in the MAS group (χ2 : 2.256, df: 2, p = 0.324). The AG genotype was significantly more frequent in the non-MAS group, while the AA genotype was significantly more frequent in the MAS group (χ2 : 11.099, df: 2, p= 0.004). Analysis of the PTX3 1449A/G polymorphism showed that individuals with the GG genotype had higher serum PTX3 levels than those with the AA and AG genotypes (p = 0.001 for both). Analysis of the PTX3 1449A/G polymorphism in patients with COVID-19 showed that those with the AG genotype were relatively more protected from MAS compared with individuals with the AA genotype. In addition, lower serum PTX3 levels are observed in patients carrying the A allele.
Subject(s)
C-Reactive Protein/genetics , COVID-19/genetics , Polymorphism, Single Nucleotide/genetics , Serum Amyloid P-Component/genetics , Adolescent , Adult , Alleles , COVID-19/pathology , Disease Progression , Female , Genotype , Humans , Macrophage Activation Syndrome/etiology , Macrophage Activation Syndrome/genetics , Male , Middle Aged , Risk Factors , Severity of Illness Index , Young AdultSubject(s)
COVID-19/pathology , Epigenesis, Genetic/genetics , Macrophage Activation Syndrome/pathology , Macrophages/immunology , p38 Mitogen-Activated Protein Kinases/metabolism , Humans , Immunity, Innate/genetics , Immunity, Innate/immunology , Lung/pathology , Macrophage Activation Syndrome/genetics , Respiratory Distress Syndrome/immunology , Respiratory Distress Syndrome/pathology , SARS-CoV-2ABSTRACT
Severe acute respiratory syndrome coronavirus 2 has infected over 100 million people since it appeared in Wuhan, China, just one year ago. This study aimed to evaluate the relationship between interleukin-6 (IL-6) gene polymorphisms -174G/C and -597G/A and coronavirus disease 2019 (COVID-19) course. The study included 70 patients aged 18-45 years who were diagnosed with COVID-19 in Turkey between March and November 2020 and hospitalized in our hospital. Of these, 40 patients required intensive care admission due to macrophage activation syndrome (MAS), and 30 patients did not develop MAS or acute respiratory distress syndrome. The frequencies of the IL-6-174G/C and -597G/A polymorphisms were determined. There were significant differences between the groups in terms of the -174G/C allele and genotype frequency according to the Hardy-Weinberg equilibrium (χ2 = 10.029, df = 1, P = 0.002 and χ2 = 9.998, df = 1, P = 0.002, respectively). The frequency of the GG genotype was significantly higher in the MAS group than in the non-MAS group (P = 0.002). The G allele was also significantly more frequent in the MAS group than in the non-MAS group (P = 0.032). Analysis of the -174G/C polymorphism in patients with MAS showed that the G allele may be a risk factor for increased serum IL-6 levels and progression to MAS.