Cv

Veronica Nuccetelli, 26 years old is a first-year PhD student in Biochemistry at the Molecular Microbiology and Structural Biochemistry (MMSB) research unit in Lyon, within the Retrovirus and Structural Biochemistry team. She earned a Master's degree in Pharmaceutical Chemistry from Sapienza University of Rome in July 2024, graduating with honors (110/110 cum laude). She began her PhD in October 2024.
Between October 2023 and March 2024, during her Master 2 thesis at the MMSB, she worked on two projects: the biochemical characterization of the interaction between the UPF1 helicase/translocase—an essential factor in the nonsense-mediated mRNA decay (NMD) pathway—and the nucleocapsid protein of SARS-CoV-2, as well as the study of the human SAMD9L protein. She primarily focused on the biochemical aspects of the UPF1 project and presented a poster on this work at the SifrARN conference in November 2024.
Her PhD research builds upon her previous work on SAMD9L, a human protein whose structure remains unknown. This protein plays multiple cellular roles, including a key function in the antiviral response to HIV, and is implicated in several genetic diseases. However, its cellular mechanisms and structural characteristics remain largely unexplored. The objective of her research is to resolve its structure and elucidate its mechanisms of action. She initially presented this project at the DyNAVir congress in Lyon in March 2024.

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 the HTLV-1 Rex protein interferes with CRM1-dependent export of UPF1, a key player in nonsense-mediated mRNA decay (NMD), an antiviral pathway. UPF1 is retained in the nucleus upon infection, and this phenotype correlates with a defect in NMD activation. There is a disruption in UPF1 binding to cellular mRNA. Paradoxically, however, UPF1 is also a component of the gag viral mRNP and plays a role in orchestrating a proviral function at different stages of the viral lifecycle. This finding reveals a coordination between antiviral and proviral functions. His research also showed that the SARS-Cov2 virus also inhibits NMD. The viral nucleocapsid protein sequesters UPF1 and UPF2, disrupting their protein-protein interactions. Unexpectedly, UPF1 appears to have a proviral function, as it stimulates viral replication.