Sylvain Latour

The Epstein-Barr virus (EBV) is an oncogenic virus belonging to the gamma herpes family. 2% of cancers worldwide, mostly lymphoma and carcinoma are caused by EBV. EBV exhibits a unique tropism for humans, in which it establishes for life a latent infection in B lymphocytes. Infection by EBV is one of the most common latent viral infections in humans: more than 90% of adults are infected and carriers of EBV. EBV is responsible for several inflammatory and lymphoproliferative diseases including lymphoma. Our main research activity is focused on the identification and the characterization of the genetic, molecular and immunological determinants predisposing to EBV associated lymphoproliferative diseases. 

This research is based on the study of children and young adults presenting a high susceptibility to develop severe EBV-associated diseases, as well as mouse models that recapitulate these conditions. Over the last years, we have identified several mendelian disorders highlighting key pathways required for the expansion and terminal differentiation of EBV-specific T cells, and we are developing a project to characterize the pathophysiological mechanisms underlying atypical EBV infections of T and NK cells. The lab is also interested in the characterization of primary immunodeficiencies and immune dysregulations causing defects in T cell differentiation and activation. 

In 2025-2026 with the arrival of Dr Kracker and Pr. Boutboul, we have extended our research to primary antibody and B-cell deficiencies, and Castleman lymphoproliferative diseases (CD) including multicentric CD associated with Kaposi's sarcoma-associated herpesvirus (KSHV/HHV8+) infection.  

Our current specific objectives/programs:

• Identification of genetic predisposing factors in pediatric lymphoma associated with EBV or not 
• Role of anti-IL-27 autoantibodies (AAbs) in EBV infection and others diseases and mechanisms of appearance of anti-IL-27AAbs
• Mechanisms of CTPS1 expression in T lymphocytes 
• Role of CTPS1 in autoimmunity, GVHD and cancer
• Identification of genetic determinants and mechanisms of EBV infection and persistence in T and NK lymphocytes causing Chronic Active EBV infection (CAEBV) 
• Genetic predisposing factors and molecular mechanisms underlying primary antibody deficiencies including PI3K signaling and transcription factor IRF4 activity
• Genomic drivers, immunological determinants, stromal involvement and cell transformation in unicentric (UCD) and HHV8+ multicentric CD (MCD)