Editorial: Immune response in EBV infection: from persistence to viral-associated tumours

Since its discovery in 1964 by Anthony Epstein and his co-workers Yvonne Barr and Bert Achong (1), the Epstein Barr virus (EBV) has drawn the attention of tumor virologists, due to its unique biological behavior. In most individuals, the virus infects the host and establishes a latent infection for life as a harmless passenger, maintaining a delicate and dynamic balance with the immune system of healthy carriers (2). While primary infection, particularly in children is often clinically silent (3), viral persistence depends on finely tuned immune surveillance, and its dysregulation may culminate in chronic inflammation, autoimmunity, or malignancy (4). There is a complex interplay between EBV-related pathologies and immune response, often reflecting an imbalance in this equilibrium (5-9).The contributions gathered in this Special Issue illustrate the long way from the first stage of EBV infection through the development of EBV-associated diseases that disrupts the balance between the virus, ultimately advancing our understanding of these conditions. Together, these five studies expand our understanding of immune heterogeneity across the life course, antiviral antibody landscapes, micronutrient-immune-virus interactions, inborn errors of immunity predisposing to EBV pathology, and the spatial organization of the tumor microenvironment in EBV-driven lymphomas.In this Special Issue, Nalwoga et al (10) provide a population-level immunological framework for interpreting EBV persistence in endemic settings. By characterizing age-associated changes in innate and adaptive immune compartments, the authors reveal that immune architecture is dynamically remodeled across the lifespan under the influence of chronic pathogen exposure. In a region where EBV infection occurs early in life and coexists with multiple environmental challenges, shifts in T cell differentiation states, activation markers, and functional capacity may influence antiviral control. Age-related immune remodeling may therefore determine the balance between latent infection and pathological reactivation.