Fiche publication
Date publication
septembre 2026
Journal
Cell reports
Auteurs
Membres identifiés du Cancéropôle Est :
Pr DELECLUSE Henri-Jacques
Tous les auteurs :
Vo DNK, Chang CT, Ho HPT, Huang HH, Poirey R, Wu LS, Lim YY, Delecluse HJ, Tsai MH
Lien Pubmed
Résumé
The Epstein-Barr virus (EBV) establishes lifelong B cell infection via oral transmission; however, it paradoxically drives carcinomas in anatomically distant organs with striking geographic disparities. While genomic studies frequently link specific EBV variants to these epithelial cancers, the mechanisms bridging ubiquitous infection to distant, strain-dependent malignancies remain largely unresolved. Using an induction-free primary B cell system, we identify a circulating B cell-vector pathway driving immortalized epithelial dissemination. We demonstrate that B cells infected with carcinoma-associated strains exhibit markedly higher epithelial transmission compared with those carrying lymphoid strains. This contact-dependent process requires spontaneous lytic reactivation, viral DNA replication, and de novo virion production. Crucially, those infected B cells retain their transmission capacity for months, supporting sustained epithelial seeding. Mechanistically, entry requires gH/gL engagement of EphA2/desmocollin-2 (DSC2), with actin- and PI3K-dependent endocytosis. These findings define a lytic-coupled, receptor-dependent pathway by which the EBV exploits B cells to access the epithelium, offering a mechanistic framework for understanding strain tropism and host-virus interactions.
Mots clés
B cell vector, CP: immunology, CP: microbiology, DSC2, EBV, EBV-infected B cell, EphA2, Epstein-Barr virus, cell-to-cell transmission, epithelial infection, lytic reactivation, viral dissemination
Référence
Cell Rep. 2026 09 17;45(10):118018
