Epstein-Barr virus hijacks B cell metabolism to establish persistent infection and drive pathogenesis. Bojana Müller-Durovic

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Trends Immunol. 2024 Dec 20:S1471-4906(24)00296-5. doi: 10.1016/j.it.2024.11.011. Online ahead of print.

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.

PMID:39709272 | DOI:10.1016/j.it.2024.11.011

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