Epstein-Barr virus (EBV), a ubiquitous gammaherpesvirus, is implicated in a wide spectrum of human diseases, ranging from infectious and inflammatory conditions to autoimmune disorders and malignancies. Beyond its well-established role in viral persistence and oncogenesis, growing evidence suggests that EBV infection can profoundly reshape host cell metabolism, thereby influencing cell survival, immune signaling, inflammatory responses, and disease progression. However, the molecular and cellular mechanisms underlying EBV-induced metabolic reprogramming remain incompletely understood, and their relevance across different disease settings is still emerging.
Recent studies indicate that metabolic alterations triggered by viral infection are not merely byproducts of infection, but active drivers of host-pathogen interactions. In the context of EBV, such changes may affect epithelial cells, immune cells, and the tissue microenvironment, with downstream consequences for immune activation, macrophage polarization, chronic inflammation, and pathological remodeling. While important progress has been made in defining EBV-associated disease phenotypes, critical gaps remain in linking metabolic signatures to mechanistic outcomes and clinical manifestations.
This Research Topic aims to bring together clinical and experimental studies that explore how EBV infection reprograms host metabolism and how these changes contribute to disease pathogenesis, immune modulation, and therapeutic vulnerability. We welcome work spanning mechanistic studies, translational research, and clinical investigations across diverse disease contexts, including but not limited to inflammatory bowel disease, ulcerative colitis, lymphoproliferative disorders, epithelial diseases, autoimmune conditions, and EBV-associated cancers.
To advance understanding of the molecular and cellular basis of EBV-driven metabolic alterations, we welcome articles addressing, but not limited to, the following themes:
- Characterization of metabolic signatures induced by EBV infection in epithelial, stromal, or immune cells - Mechanistic studies of how EBV-driven metabolites or metabolic pathways regulate immune responses and inflammatory signaling - The role of metabolic reprogramming in macrophage polarization, monocyte activation, and immune microenvironment remodelin - In vitro, organoid, animal, and multi-omics models for studying EBV-associated metabolic-host interactions - Clinical studies linking EBV-related metabolic alterations to disease severity, progression, or treatment response - Identification of diagnostic biomarkers and therapeutic targets related to EBV-induced metabolic pathways - Comparative analyses of EBV-driven metabolic and immunologic changes across inflammatory, autoimmune, and neoplastic diseases
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Article types
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
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