2017- : Team leader, Institut de Recherche en Infectiologie de Montpellier (IRIM), Montpellier, France
2012-2016: ATIP-Avenir group leader in François Clavel's U941 unit, Hôpital Saint- Louis, Paris
2009-2012: Principal investigator in Pierre Charneau's laboratory, Institut Pasteur, Paris
CNRS recruitment (CR1): 1st October 2009
2007-2009: Post-doc fellow in Frank Kirchhoff's laboratory, Ulm University, Germany
Habilitation diploma: 10th November 2009
Title "Infection and manipulation of human and simian cells by HIV and other primate lentiviruses"
2002-2007: Post-doc fellow in Pierre Charneau's laboratory, Institut Pasteur, Paris
1998-2002: PhD student in Chris Paraskeva's laboratory, Bristol University, UK
PhD diploma: 7th March 2002
Title "Interaction with the retinoblastoma protein modulates the subcellular localisation of BAG-1 in human colonic epithelial cells: implication for apoptosis"
Our work focuses on viral trafficking and nuclear import, with particular focus on HIV. Historically, the team has focused on viral determinants of nuclear import, for instance by characterising the nuclear import defect of HIV-1 lacking the DNA flap (Iglesias et al., 2011). More recently however, our work interest has turned to the cellular biology of retroviral infections, by contributing to a better understanding of how proteins of the nuclear pore and of the cytoskeleton promote HIV-1 infection. In particular, we showed that the nucleoporin Nup358/RanBP2 acts as a docking site for HIV-1 capsid at the nuclear pore (Di Nunzio et al., 2012), and that microtubule-associated proteins MAP1A and MAP1S mediate interaction of HIV-1 capsid with microtubules thus promoting retrograde transport (Fernandez et al., 2015). In collaboration with C. Zimmer (Institut Pasteur, Paris) we developed a PALM super-resolution microscopy approach (FlAsH-PALM) that allows the volume of HIV capsids in the cytoplasm of infected cells to be probed by labelling integrase (Lelek et al., 2012).
The team is also interested in restriction of retroviral infections. In collaboration with S. Nisole (Faculté des Saints-Pères), we showed that TRIM5α is a SUMO substrate (Dutrieux et al., 2015), and that TRIM5α is inactivated in dendritic cells as a result of SUMOylation-dependent nuclear sequestration that promotes sensing of retroviral infections (Portilho et al., 2016).