Bojana Müller-Durovic, Jessica Jäger, Glenn R Bantug, Christoph Hess
{"title":"Epstein-Barr virus hijacks B cell metabolism to establish persistent infection and drive pathogenesis.","authors":"Bojana Müller-Durovic, Jessica Jäger, Glenn R Bantug, Christoph Hess","doi":"10.1016/j.it.2024.11.011","DOIUrl":null,"url":null,"abstract":"<p><p>When B cells engage in an immune response, metabolic reprogramming is key to meeting cellular energetic and biosynthetic demands. Epstein-Barr virus (EBV) is a highly prevalent gamma-herpesvirus, latently infecting B cells for the human host's lifetime. By hijacking signaling pathways of T cell-dependent humoral immunity, EBV activates B cells in a T cell-independent manner, forcing lymphoblastoid transformation. Interlinked with this coercion of signaling pathways, EBV has also evolved strategies to manipulate B cell metabolism. In this opinion article we integrate recent findings from studies of B cell metabolic reprogramming after EBV infection and during antigen-specific activation, respectively. We hypothesize that defining EBV host-cell metabolic vulnerabilities that differ from pathways required for B cell immunity might uncover novel therapeutic targets against EBV-related diseases.</p>","PeriodicalId":54412,"journal":{"name":"Trends in Immunology","volume":" ","pages":"7-16"},"PeriodicalIF":13.1000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Trends in Immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.it.2024.11.011","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/20 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
When B cells engage in an immune response, metabolic reprogramming is key to meeting cellular energetic and biosynthetic demands. Epstein-Barr virus (EBV) is a highly prevalent gamma-herpesvirus, latently infecting B cells for the human host's lifetime. By hijacking signaling pathways of T cell-dependent humoral immunity, EBV activates B cells in a T cell-independent manner, forcing lymphoblastoid transformation. Interlinked with this coercion of signaling pathways, EBV has also evolved strategies to manipulate B cell metabolism. In this opinion article we integrate recent findings from studies of B cell metabolic reprogramming after EBV infection and during antigen-specific activation, respectively. We hypothesize that defining EBV host-cell metabolic vulnerabilities that differ from pathways required for B cell immunity might uncover novel therapeutic targets against EBV-related diseases.
期刊介绍:
Trends in Immunology serves as a vital platform for tracking advancements across various areas of immunology, offering concise reviews and hypothesis-driven viewpoints in each issue. With additional sections providing comprehensive coverage, the journal offers a holistic view of immunology. This broad perspective makes it an invaluable resource for researchers, educators, and students, facilitating the connection between basic and clinical immunology. Recognized as one of the top monthly review journals in its field, Trends in Immunology is highly regarded by the scientific community.