Over the past three decades, one third of (re)emerging viral diseases were caused by arboviruses, which are pathogens transmitted from arthropod vectors to vertebrate hosts upon blood feeding. Rift Valley fever virus (RVFV) spread within a few decades from Eastern to whole Africa, Indian ocean (1990) and Arabian Peninsula (2000). RVFV strains harbor an overall low genetic diversity compare to other arboviruses, with some mutations having a major impact on RVFV infection. Two RVFV strains, MRU25010-30 and MRU2687-3 isolated from infected animals during the 2010-2013 outbreak in Mauritania, displayed a relatively similar genetic make-up but a marked difference in host virulence. In mice, MRU25010-30 triggered a faster death compare to MRU2687-3 (Chabert et al., 2024). Reverse genetics (RG) showed that MRU25010-30 higher replication rate was associated with two point mutations in the 5′ UTR and the envelope protein Gn encoding gene of the M segment, respectively. My PhD project focuses on the viral determinants governing mosquito vector competence for RVFV. To this end, Culex quinquefasciatus and Aedes aegypti mosquitoes were exposed to an infectious blood meal spiked with selected RG RVFV strains, including RG MRU25010-30 with the 5’ UTR or Gn mutations mentioned above. Our results indicate that, in addition to host infection, the 5' UTR point mutation within the M segment also plays a key role in vector infection. These data highlight that mosquito infection and ultimately vector competence is strongly influenced by the genotype of RVFV circulating field strains.