Epstein-Barr (EBV) has the ability of long-life persistence in the human body; it exists in latent form in immunocompetent cells and can be reactivated under the influence of different exo- and endogenous unfavorable factors. Specific tropism of the virus to immunocompetent cells can influence their expression level of microRNA, which are active regulators of immune response. The purpose of the study was to conduct a comparative assessment of miR-146A and miR-155 expression level. Material and methods. The comparative assessment was conducted in two groups of patients with allergopathy in combination with active (1st group) and latent (2nd group) phases of chronic Epstein-Barr virus infection and control group of healthy individuals. Patients underwent clinical, general laboratory, instrumental, specific allergic, molecular genetic studies, cytological examination of the smear from the nasal mucosa. Skin tests were performed with allergen extracts (Diater, Spain). An assessment of the functional state of the lungs was performed on the basis of spinography (Vitalograph ALPHA No. AL011734, Germany). Clinical diagnosis of AR and / or BA was based on the criteria of ARIA (2016), GINA (2016-2017). To determine the general and specific IgE (sIgE) to EBV (EBNA-IgG, EBV-VCA-IgG) antigens and specific antibodies, we used an immunoassay with the Euroimmun test system, Germany, according to the manufacturer's instructions. Determination of DNA of Epstein-Barr virus infection in blood, saliva and mucous membrane of the pharynx was performed the polymeric chain reaction method on AmpliSens diagnostic sets using Rotor Genе 6000 (Corbett Recearch, Australia). Results and discussion. The study results showed that in latent phase, Epstein-Barr virus infection used own mechanisms of latency to avoid immune response, which was characterized by increased synthesis of miR-155 and miR-146A compared with control group. However, the opposite vector of changes of these microRNAs with antagonistic properties was observed compared with active phase. In active phase of Epstein-Barr virus infection, this direction of changes only intensified and was associated with acute manifestations of allergopathy. Patients in the 2nd group also showed higher levels of miR-155, although without a significant difference with the control group, while patients in the 2nd group were characterized by a history of pollen allergy with a history of broncho-obstruction syndrome, blood eosinophilia and nasocytogram. In our opinion, the imbalance between miR-155 and miR-146a, which Epstein-Barr virus infection created to provide a phase of lation, contributed to the chronicity of the allergic inflammatory process. Our conclusion confirmed the data of Okoye and colleagues about the antagonistic role of miR-155 and miR-146a in the regulation of the immune response administered by Th2. Conclusions. The chronic Epstein-Barr virus infection in patients with allergopathy had different influence on miR-155 and miR-146A levels depending on the phase of virus persistence. The increase in the expression of miR-155 initiated an inadequate antiviral response from the side of both humoral and cellular immunity, enhanced cell-mediated inflammation, working unison with miR-146a.
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