Main immunogenetic, pathogenetic, and clinical features of Epstein-Barr virus infection (literature review)

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.

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Journal
Inter Collegas
Published
2025-06-30
DOI
https://doi.org/10.35339/ic.2025.12.2.css
Primary Topic
Viral-associated cancers and disorders
Type
article
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article

Main immunogenetic, pathogenetic, and clinical features of Epstein-Barr virus infection (literature review)

Oleksandr Saienko, Mykola Dmytrovych Chemych, Oksana Mykolaivna Chemych, В. С. Світайло et al.
Inter Collegas
Viral-associated cancers and disorders
article

Main immunogenetic, pathogenetic, and clinical features of Epstein-Barr virus infection (literature review)

Oleksandr Saienko, Mykola Dmytrovych Chemych, Oksana Mykolaivna Chemych, В. С. Світайло, N. Klymenko
article en

Abstract

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.

Inter CollegasVol. 12(2)
Sumy State University (UA)
Openalex Percentile: Top 68%
Viral-associated cancers and disorders
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