Epstein-Barr Virus (EBV), or human herpesvirus type 4, is a common pathogen that infects 90–95% of the adult population worldwide. Over the past 10 years, research has significantly expanded our understanding of the etiological characteristics of EBV infection, its role in the development of malignant and autoimmune diseases, and its mechanisms of interaction with the immune system. EBV is a complex herpesvirus that has the ability to infect B lymphocytes and epithelial cells, ensuring lifelong persistence in the human body. It has two phases in its life cycle – lytic and latent in which different genetic programs and immune mechanisms are activated. Depending on the functional state of the cell and the type of latency, the virus can change gene expression patterns to avoid immune surveillance. The immune response to EBV infection includes humoral and cellular components. Cytotoxic CD8⁺ T lymphocytes play a decisive role, but the virus is able to effectively modulate or suppress their activity. To ensure long-term persistence, the virus employs a number of immune evasion strategies, including disruption of antigen presentation via major histocompatibility complex I and II molecules, induction of regulatory T cells, and suppression of proinflammatory responses. EBV infection can manifest in various clinical forms, from infectious mononucleosis to severe chronic diseases: chronic active EBV infection, post-transplant lymphoproliferative disorders, and EBV-associated neoplasms. There is a close relationship between EBV and the development of certain autoimmune diseases, including rheumatoid arthritis, Sjögren's syndrome, and systemic lupus erythematosus. The virus is capable of causing immune dysregulation through molecular mimicry, expression of viral proteins, activation of cytokine pathways, and loss of immune tolerance. Keywords: pathogenesis, clinical presentation, autoimmune processes, oncogenicity, robust health and well-being.
Chemych et al. (Mon,) studied this question.