Abstract

In the research data on the study of interconnection between polymorphism of HLA DRB1 genes and the risk of HIV infection and co-infection and HIV/tuberculosis are presented.The cohort of observation was HIV-infected individuals with different clinical stages aged from 24 to 58 years, average age being 38 years. 90 patients (89.2%) received HAART.There were 32 (31.4%) HIV-infected patients with manifestations of tuberculosis, 70 (68.6%) HIV patients without manifestations of tu­ber­culosis. Among the cohort of HIV-infected patients with manifestations of tuberculosis, pulmonary forms of tuberculosis was in 32 (100%), of which extrapulmonary forms of tuberculosis were in 12 (37.5%) patients. The majority of cases of tuberculosis occurred in HIV-infected patients in the IV clinical stage. Among HIV-infected patients, the following alleles of the HLA gene DRB1 *01 (10%) *04 (10%) *07 (13%), *11 (15%), *13 (13%), *15 (10%) occurred more often, HLA DRB1 *03 *08 *09 *10, *12, *14, *16, * 17, *18 were rarely found (1-7%). Similar distributions of DRB1 genes were noted among residents of the region with the dominance of HLA DRB1 *01 *04 *07 *11 *13 and *15. With the presence of alleles of the locus DRB1 *13, DRB1 *03 and DRB1 *08, the greatest probability of co-infection of tuberculosis was observed in HIV-infected patients. The risk of tuberculosis is by 2 times higher with a significant difference in HIV-infected patients with DRB1 *13 locus alleles, DRB1 *03 – by 4.4 times and DRB1 *08 – by 5.4 times. Significant chances of tuberculosis occurrence are higher – by 2.6 times in HIV-infected patients with DRB1 *13 locus alleles, DRB1 *03 – by 5.1 times and DRB1 *08 – by 6.4 times. Thus, the variability of the HLA DRB1 locus alleles may play a predisposing or protective role in the occurrence of tuberculosis in HIV-infected patients.

Highlights

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  • Ʉɨɝɨɪɬɭ ɧɚɛɥɸɞɟɧɢɹ ɫɨɫɬɚɜɢɥɢ ȼɂɑ-ɢɧɮɢɰɢɪɨɜɚɧɧɵɟ ɩɚɰɢɟɧɬɵ ɫ ɪɚɡɥɢɱɧɵɦɢ ɤɥɢɧɢɱɟɫɤɢɦɢ ɫɬɚɞɢɹɦɢ ɜ ɜɨɡɪɚɫɬɟ ɨɬ 24 ɞɨ 58 ɥɟɬ, ɫɪɟɞɧɢɣ ɜɨɡɪɚɫɬ ɤɨɬɨɪɵɯ ɫɨɫɬɚɜɢɥ 38 ɥɟɬ. ɉɨɥɭɱɚɥɢ ȼȺȺɊɌ 90 ɩɚɰɢɟɧɬɨɜ (89,2%). ȼɂɑ-ɢɧɮɢɰɢɪɨɜɚɧɧɵɯ ɩɚɰɢɟɧɬɨɜ ɫ ɩɪɨɹɜɥɟɧɢɹɦɢ ɬɭɛɟɪɤɭɥɟɡɚ ɛɵɥɨ 32 (31,4%), ȼɂɑ ɛɟɡ ɩɪɨɹɜɥɟɧɢɣ ɬɭɛɟɪɤɭɥɟɡɚ ɫɨɫɬɚɜɢɥɢ 70 (68,6%) ɩɚɰɢɟɧɬɨɜ. ɋɪɟɞɢ ɤɨɝɨɪɬɵ ȼɂɑɢɧɮɢɰɢɪɨɜɚɧɧɵɯ ɩɚɰɢɟɧɬɨɜ ɫ ɩɪɨɹɜɥɟɧɢɹɦɢ ɬɭɛɟɪɤɭɥɟɡɚ ɥɟɝɨɱɧɵɟ ɮɨɪɦɵ ɬɭɛɟɪɤɭɥɟɡɚ ɢɦɟɥɢ 32 (100%), ɢɡ ɧɢɯ ɜɧɟɥɟɝɨɱɧɵɟ ɮɨɪɦɵ ɬɭɛɟɪɤɭɥɟɡɚ ɛɵɥɢ ɭ 12 (37,5%) ɩɚɰɢɟɧɬɨɜ

  • Ɜɚɪɢɚɛɟɥɶɧɨɫɬɶ ɚɥɥɟɥɟɣ ɥɨɤɭɫɚ HLA DRB1 ɦɨɠɟɬ ɢɝɪɚɬɶ ɩɪɟɞɪɚɫɩɨɥɚɝɚɸɳɭɸ ɢɥɢ ɡɚɳɢɬɧɭɸ ɪɨɥɶ ɜ ɜɨɡɧɢɤɧɨɜɟɧɢɢ ɬɭɛɟɪɤɭɥɟɡɚ ɭ ȼɂɑ-ɢɧɮɢɰɢɪɨɜɚɧɧɵɯ ɩɚɰɢɟɧɬɨɜ

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Summary

ɄɅȱɇȱɑɇȺ ɆȿȾɂɐɂɇȺ

Ɋɟɮɟɪɚɬ +/$ '5% ɩɨɥɢɦɨɪɮɢɡɦ ɢ ɪɢɫɤ ɜɨɡɧɢɤɧɨɜɟɧɢɹ ɤɨɢɧɮɟɤɰɢɢ ȼɂɑɬɭɛɟɪɤɭɥɟɡ ɒɨɫɬɚɤɨɜɢɱ Ʉɨɪɟɰɤɚɹ ɅɊ ȼɨɥɢɤɨɜɚ ɈȺ Ʌɢɬɜɢɧ ȿɘ Ƚɭɛɚɪɶ ɂȺ Ʉɭɲɧɟɪɨɜɚ ȿȺ ɒɟɜɟɥɟɜɚ ȿȼ ȼ ɪɚɛɨɬɟ ɩɪɟɞɫɬɚɜɥɟɧɵ ɞɚɧɧɵɟ ɢɡɭɱɟɧɢɹ ɜɡɚɢɦɨɫɜɹɡɢ ɦɟɠɞɭ ɩɨɥɢɦɨɪɮɢɡɦɨɦ ɝɟɧɨɜ HLA DRB1 ɢ ɪɢɫɤɨɦ ɜɨɡɧɢɤɧɨɜɟɧɢɹ ɢ ɬɟɱɟɧɢɟɦ ȼɂɑ ɢ ɤɨ-ɢɧɮɟɤɰɢɢ ȼɂɑ/ɬɭɛɟɪɤɭɥɟɡ. The risk of tuberculosis is by 2 times higher with a significant difference in HIV-infected patients with DRB1 *13 locus alleles, DRB1 *03 – by 4.4 times and DRB1 *08 – by 5.4 times. Significant chances of tuberculosis occurrence are higher – by 2.6 times in HIV-infected patients with DRB1 *13 locus alleles, DRB1 *03 – by 5.1 times and DRB1 *08 – by 6.4 times. The variability of the HLA DRB1 locus alleles may play a predisposing or protective role in the occurrence of tuberculosis in HIV-infected patients. Ɍɚɛɥɢɰɹ 1 ɑɚɫɬɨɬɚ ɡɭɫɬɪɿɱɚɥɶɧɨɫɬɿ ɬɭɛɟɪɤɭɥɶɨɡɭ ɭ ȼȱɅɿɧɮɿɤɨɜɚɧɢɯ ɩɚɰɿɽɧɬɿɜ ɡ ɪɿɡɧɢɦɢ ɚɥɟɥɹɦɢ ɥɨɤɭɫɭ +/$ '5%

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