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The Epstein–Barr virus, which is persistent in the human organism throughout lifetime after the primary infection, is involved in the pathogenesis of a number of somatic chronic diseases. It is known that the virus successfully escapes the immune control, and has many mechanisms to regulate the components of immune system s as well. In our work, we summarized the current scientific data on the effect of the persistent Epstein-Barr virus on the function and quantity of T- and B-lymphocytes, NK cells, activity of the toll-like receptors, secretion of interleukins, interferons and other cytokines. The immunity dysfunction with the immunoactivation predominance leads to the formation of severe forms of chronic active Epstein–Barr virus infection such as the chronic mononucleosis, hemophagocytic lymphohistiocytosis. The immunosuppression is characteristic for the atypical course of the chronic active Epstein–Barr virus infection. The ability of some viral proteins to antigenic mimicry (that is, the homology of viral and human proteins) is the determining factor in the development of the chronic fatigue syndrome, multiple sclerosis and systemic lupus erythematosus. The Epstein–Barr virus is capable of the immortalization of the B-lymphocytes, including the autoaggressive ones, which leads to the formation of the chronic autoimmune diseases. Study of the development mechanisms of these diseases permits to develop the new, more effective, personalized prevention and treatment schemes, for example, using the targeting therapy.
Yakushina et al. (Wed,) studied this question.
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