Léa PROCHASSON Cv:

Léa PROCHASSON is a young researcher whose scientific curiosity and strong interest in interdisciplinary topics have shaped a multidisciplinary career combining biochemistry, virology, and oncology. Passionate about molecular and cellular dynamics, she first completed a Doctor of Pharmacy (PharmD) degree at the University of Tours, following work on histone-modifying complexes, and subsequently obtained a PhD in Integrative and Cellular Molecular Biology at ENS de Lyon, under the supervision of Vincent Mocquet in the PRIO team (Post-transcriptional Regulation in Infection and Oncogenesis). During these three years, she focused on the post-transcriptional regulation of cellular and viral RNAs by characterizing the impact of dysregulation of the Nonsense-Mediated Decay (NMD) pathway on host–pathogen interactions, in the context of infections by the retroviruses HTLV-1 and HIV-1. She then joined the “Non-coding RNAs, Epigenetics and Genome Plasticity” team led by Antonin Morillon at the Institut Curie, where she is currently pursuing her work on RNA through a translational research project. Her research focuses on the immunogenic potential of non-coding RNAs, particularly through their characterization as potential sources of peptide candidates for therapeutic anti-cancer vaccines. Driven by a constant desire to learn and to share knowledge, she is also actively involved in student supervision and teaching.

Makram Mghezzi-Habellah Cv:

Makram, 27 years old, completed his Bachelor's degree and the first year of his Master's at the University Claude Bernard of Lyon I. His studies focused on genetics and cellular biology. During this period, he developed an increasing interest in RNA biology and viral RNA, leading him to pursue a specialized diploma in these fields at Paris University, where he also completed his internship. During his PhD, he focused on studying the consequences of viral infections on host cell homeostasis. He investigated two RNA viruses, SARS-CoV-2 and HTLV-1. Makram's research demonstrated that HTLV-1 Rex interferes with CRM1 dependent export of UPF1, a key player in non-sense mediated decay (NMD). For SARS-CoV-2, he reported that the virus also inhibits NMD. And unexpectedly, UPF1 seems also to have proviral function because it stimulates viral replication.