ABSTRACT
Background: Cytokines are signaling molecules and involve lymphocytes and macrophages in the immune response. Lymphocyte-platelet adhesion is one of the mechanisms that ensure the cooperation of various subpopulations of cells and allow them to migrate through the vascular wall into the tissue. Aim(s): To study the function of lymphocyte-platelet adhesion depending on SNP of IL-2 (T330G) gene in healthy subjects and patients with COVID-19. Method(s): The research involved 168 patients with COVID-19 and 100 healthy people of the same age and gender. The participants of the study were Caucasian race and lived in the Trans-Baikal Territory. The examine of LPA was carried out by the method of Yuri Vitkovsky et al. (1999). The SNP of IL-2 (T330G) gene was determined by PCR. Such methods as Equilibrium Hardy-Weinberg, chi2-test, odds ratio descriptive statistics and the mean values (M) and standard deviation (SD) were used. Statistical significance was measured at the value p < 0.05. Result(s): We found all the studied IL-2 mutations in accordance with the Hardy-Weinberg law (p>0.05). The heterozygous T/G of IL-2 gene was registered significantly more frequently in the group of patients in comparison with the control group. Based on the obtained data on frequency distribution, the chance of developing SARS-COV- 2 increased in carriers of the allele T and the T/T genotype of IL-2 gene (p < 0.001). It was found that patients with SARS-COV- 2 had an increase in the LPA index compared to the group of healthy individuals (15.2 +/- 1.1%). The maximum amount of LPA was detected among patients with T/T genotype -39.7 +/- 2.1%, the minimum amount -in the owners of G/G (31.4 +/- 1.9%) (p< \0.001). Conclusion(s): 1) SARS-COV- 2 is accompanied by an increase in LPA function indicators, which depend on SNP of IL-2 (T330G) gene. 2) Carriers of allele T and T/T genotype of IL-2 gene (T330G) predispose to the development of COVID-19.
ABSTRACT
Background : Lymphocyte-platelet adhesion (LPA) is the ability of lymphocytes with CD3 + , CD4 + , CD16 + cell surface markers to form coaggregates with platelets using adhesion molecules, that allows lymphocytes to adhere to the damaged endothelium and migrate into the damaged surface of the vascular wall. Aims : Investigation of the amount of lymphocyte-platelet aggregates and lymphocyte-platelet clusters in patients with COVID-19. Methods : The research involved 168 patients with SARS-CoV-2 (COVID-19) and 100 healthy people of the same age and gender. Patient ' s blood samples were taken on the 1st-2d, 10th-12th, 21st-24th days. The participants of the study were Caucasian race and lived in the Trans-Baikal Territory. The examine of LPA was carried out by the method of Yuri Vitkovsky et al. (1999). The number of lymphocyte-platelet clusters (LPC) was estimated and expressed in rel. units per 100 free-standing cells. The results were expressed in averages and the standard deviation (M ± SD) was calculated. Significant differences were considered for P < 0.05. Results : The authors revealed that on the 1st-2d day of disease among patients the number of LPA increased to 28.9 ± 3.2%, LPC -to 5.0 ± 2.3% as compared with the control group ( P < 0.001). The average platelets volume LPA-rasio also increased by 2.9 times ( P < 0.05). Among patients during 10-12 days of the disease there was a notable increase of LPA and LPA-rasio up to 41.3 ± 1.9% and 5.8 ± 0.48 respectively (higher by 3 times as compared to the control group). On the 21-24th days of the disease with patients being in the hospital, there were no significant differences in the studied parameters among the patients and the control group. Conclusions : There is an increase in the ability of lymphocytes to adhere platelets to their surface and contact with other lymphocytes while forming clusters in the acute phase of COVID-19. Probably the process of clustering is mediated by platelet and leukocyte adhesive molecules.