Le jeudi 4 juin 2026, Monsieur Arthur PONCELET, titulaire d'un Master en Médecine (ULB) et d'un Certificat de formation à la recherche en sciences médicales présentera l'examen en vue de l'obtention du grade de Doctorat en sciences médicales sous la direction de Madame Bénédicte MACHIELS et de Monsieur Stanislas GORIELY (ULB). Le doctorat est réalisé en co-tutelle avec l'ULB.

Cette épreuve consistera en la défense publique d'une thèse intitulée : "Deciphering the impact of gammaherpesvirus infection on monocyte development and functional reprogramming". 

Le jury sera composé de :

Alain LE MOINE (ULB) (Président), Jean-Yves SPRINGAEL (ULB) (Secrétaire), Frédéric BARON, Bérangère DE LAVAL (Univ. marseille), Stanislas GORIELY (ULB), Bénédicte MACHIELS, Thomas MARICHAL, Alberto YANEZ (Univ. Valencia).

Résumé de la thèse

The immune system is continuously shaped by microorganisms, with persistent viruses exerting long-lasting effects on immune function. Gammaherpesviruses (γHVs), such as Epstein–Barr virus (EBV), establish lifelong infections and may durably imprint innate immune memory. Monocytes, which integrate environmental signals to guide their differentiation and function, are prime candidates for such reprogramming.Using Murid herpesvirus 4 (MuHV-4) infection in wild-type mice and EBV infection in humanized mice, we investigated how γHVs influence monocyte fate and function. Latent MuHV-4 infection induced sustained phenotypic, transcriptomic, and epigenetic changes in bone marrow (BM) monocytes and their progenitors, leading to reprogrammed monopoiesis and the emergence of a distinct subset of classical monocytes with dendritic cell–like features. This imprinting coincided with the accumulation of IFNγ-producing memory CD8⁺ T cells in the BM. Similar monocyte alterations were observed during EBV infection in humanized mice and correlated with activated BM CD8⁺ T cells. Integrated transcriptomic and epigenetic analyses revealed changes in chromatin accessibility involving STAT1- and IRF-dependent pathways. Functionally, reprogrammed monocytes displayed enhanced cytokine production upon low-dose LPS challenge, promoting T cell activation.Together, these findings demonstrate that latent γHV infection, through sustained IFNγ production by CD8⁺ T cells, remodels the BM niche, reprograms monopoiesis, and establishes durable changes in monocyte responsiveness, highlighting long-term adaptations of hematopoiesis that promote a novel host–pathogen equilibrium.