The antigen system on the surface of human cells is responsible for recognizing foreign antigens. In organ transplantation, the immune system reacts to all foreign antigens that are different from the recipients antigens. In practice, solid organ transplantation is carried out with varying degrees of genetic discrepancy, while the main principle that should be followed to prevent acute and chronic transplant rejection reactions is to avoid unacceptable discrepancies. As a result, the diagnosis of typing genes of histocompatibility allows you to select a donor to which the recipient will not have sensitization. The article presents an analysis of various methods for typing human histocompatibility genes for organ and tissue transplantation. The discovery of the polymerase chain reaction was a new stage in the typing of human histocompatibility genes, which made it possible to develop new methods of gene typing. As a result, methods have been developed for typing genes using sequencers, including a new-generation MiSeq sequencer (Illumina, USА), a Massarray genomic time-of-flight analyzer (Agena Bioscience, USA). The use of sequencing has led to the possibility of simultaneous typing from 24 to 100 DNA samples. Modern technological solutions have made it possible to improve the 3rd generation NGS sequencers and provide a maximum productivity of up to 30 billion nucleotides per run, minimize restrictions on the length of DNA readings, as well as track parameters, control the sequencing process and conduct base-scaling in real time. Modern data using rapid genes typing of the human histocompatibility system (MinION Oxford nanopore) meet the needs of particularly sensitive recipients. Preliminary evidence suggests that this method will be more economical and efficient and will replace all previous ones over time (8 figs, bibliography: 40 refs).

The work analyzed the polymorphisms of the HLA-DRB1 and IL28 genes in 100 patients who underwent COVID-19 with the development of infection with varying degrees of severity. To a mild degree of severity were patients without complications in the form of infectious pneumonate, to moderate and severe degrees - with the development of pneumonate with varying degrees of lung damage. In general, the distribution of alleles in patients with COVID-19 did not differ from the distribution of average values in Russia. However, the HLA-DRB1 *01 и *07 alleles were more common. Comparison of the frequency of HLA-DRB1 alleles in patients with COVID-19 with varying severity revealed more common alleles of *13 and *07 in the severety severe group. However, with OR of 3.2 and 1.8, their confidence intervals (CL) were in the range of 0.9-9.8 and 0.7-4.5 respectively. At severe severity, the presence of homozigotic variants of allele *07 is noted. (Fisher exact test, r.0.04). As for the IL28B gene, no statistically significant differences from the control group were found.

The review presents data on the importance of mitochondrial DNA in aging of cardiomocytes. The mechanisms of accumulation of mutations in mtDNA and reduction of its content, as well as the consequences of these phenomena in cardiomyocytes are described. The similarity of the aging processes of cardiomyocytes and skeletal muscle cells and comparison with the aging processes occurring in mononuclear cells of peripheral blood is indicated. The death of cardiomyocytes and skeletal muscle cells leads to the destruction of mutant forms of mtDNA, as a result of which the content of mutant forms of mtDNA, constantly increasing with age, does not exceed 1-2% of the total number of mtDNA molecules. In addition, the death of cardiomyocytes and myocytes is accompanied by the release of CpG-motive cells mtDNA, which can cause local and general inflammation in old age. It is concluded, that in the treatment of elderly patients it is desirable to take into account the degree of aging ("biological age”) of their myocardial and their presence of chronic myocarditis, for which appropriate diagnostic methods should be developed.

About 85% of all sudden death are of cardiological origin. Predisposition to sudden cardiac death is known for the young and adult patients with a hereditary heart disease that can cause sudden cardiac arrest. The purpose of the work was to study the genetic predisposition for cardiovascular diseases in people with a risk of sudden cardiac death. We examined patients aged 19,7±2,1 years with a risk of sudden cardiac death based on specific complaints and medical history, and considering the known markers of the life-threatening arrhythmias. Of the 1000 patients, 167 with a risk of sudden cardiac death were selected according to the questionnaire. In 80 randomly selected patients from this group, gene polymorphisms associated with the development of thrombophilia and hypertension were studied by real time PCR, and in 59 patients the polymorphisms of genes associated with impaired carbohydrate and lipid metabolism were studied. A number of differences were revealed according to the standard 12-channel electrocardiography in comparison with practically healthy individuals. In the study of genetic factors predisposing the development of thrombophilia, hypertension, type 2 diabetes mellitus, lipid metabolism disorders, a high percentage of hetero- and homozygous individuals was revealed by the risk allele of the PAI-1 (83.3%), ITGA2 (69.2%), AGT genes (72.5%), NOS3 (58.8%), PON1 (56%), LEPR (64.3%). The data obtained indicate a significant role of genetic factors in the development of sudden cardiac death, and the synergistic effect of genes, as a result of which the presence of a risk allele in one gene can enhance the expression of another gene.