Proceedings of the International scientific and practical conference ―Modern Science: Challenges and Perspectives‖ (February 9-11, 2026) / Publisher website: www.naukainfo.com. - London, United Kingdom, 2026. - 121 p.

109 young adults (≤21 years). Chronic EBV infection was defined as recurrent or persistent viremia lasting longer than three months, invasive EBV disease, or an EBV DNA copy number exceeding 100,000 copies in whole blood or plasma [4]. The EBV viral load in our patient’s blood (4.94 × 10⁵ copies/mL) supports the findings of this study, indicating that EBV persistence may occur in the absence of immunodeficiency or immune dysregulation. Lymphoproliferative disease may develop as a consequence of the persistence of EBV-infected lymphocytes, reflecting immune dysfunction and/or proliferation of EBV-infected lymphocytes [4]. Prolonged EBV persistence in the presence of LAP in children should therefore be considered a risk factor for the development of LPDs. A number of factors, in addition to EBV, may induce CD30 expression on the surface of lymphocytes, including reactive conditions as well as inflammatory and infectious diseases. Establishing an accurate diagnosis requires careful clinicopathological correlation, along with histological and immunohistochemical examination of lymph node biopsy specimens and, in selected cases, molecular genetic testing to determine T-cell clonality [5]. Clinicians should keep this in mind when evaluating patients with LAP. The CD30 antigen (cluster of differentiation 30), a type I transmembrane glycoprotein belonging to the tumor necrosis factor receptor superfamily 8 (TNFRSF8), was first described in Hodgkin lymphoma cells. Subsequently, the same antigen was identified in several non-Hodgkin lymphomas, including primary cutaneous anaplastic large cell lymphoma (PC-ALCL) [6]. CD30 is a membrane cytokine receptor that appears on the surface of mitogen-activated T and B lymphocytes. CD30 expression requires activation of the CD28 signaling pathway or the interleukin-4 receptor [7,8]. The pathogenesis of LPDs is as follows: CD30 interacts with its ligand CD30L (CD153, TNFSF8), a type II transmembrane glycoprotein that also belongs to the tumor necrosis factor family and is expressed on activated T lymphocytes – predominantly on the surface of CD4⁺ cells (T helper type 1 and type 2) – as well as on B lymphocytes and certain other immunocompetent cells, including antigen-