Positions and Honors
Positions and Employment
1984-1984: Assistant Director of Emergency Room - University Hospital of Caracas, Venezuela
1984-1987: Associate Professor in the “Cancerology and Immunogenetic Institute (Unité Associée CNRS n°1163)
1987-1988: Associate Professor in the “Laboratory of Immunogetic of Allotransplantation
(INSERM U 267)”
1988-2002: Associate Professor in the “Immunohematology and Immunopathology Unit, Institut
2002 to present: Associate Professor and team leader in the “Retrovirus Biology Unit, Institut Pasteur”
1988-1990 Teaching: Lectures in Immunopathology.
1994-1997 Teaching: Lectures in Immunology.
1998-2002 Teaching: Director of Immunology Lectures in Institut Pasteur.
1995 to present Teaching: Lectures in Immunology for administration staff.
1995-1996 Teaching: Virology: Virokines and immune evasion (Paris V)
2003 to present Teaching: Immunology: Immune cellular responses against virus (ParisVI).
2003 to present Teaching: Fungal Diseases: Immunological responses against fungi (Paris V)
2005 Teaching: Immunology course in Vietnam.
2006 Teaching Immunology course in Romania
2007 Teaching Immunology course in Uruguay
2008 Teaching Immunology course in Mexico
2008 Teaching Immunology course in Hong Kong
2009 Teaching Immunology course in Hong Kong
2010 Teaching Immunology course in Hong Kong
2010 Teaching Immunology course in Mexico
1998 Scientific member of "Advisory Commission of the Valorisation of Research"
1999 to present Scientific member of "Innate immunity and VIH group", ANRS
2000 to present Scientific Consultant of "Sedac Therapeutics"
2003 to present Scientific member of “ Scientific Committee 1: Interaction host-virus”, ANRS
2000 to present Editorial Board of Transcriptase (French HIV review journal for medical doctors).
2004 to present President of Texcell Scientific Committee
2005 to present Coordinator of Latin America cooperation
Supervision of 3 Postdoctoral 5 Ph.D, 4 Master, 7 undergraduate students
1996 Orden del Libertador clase I (Venezuela)
I centred my work on the role of cells NK in protection against the infection by the HIV-1 in particular by the study of the activity of NK cells and the secretion of cytokines. Our studies in exposed to the HIV but not infected individuals (EUs) showed no difference of percentages or absolute values of circulating NK cells was observed in EUs compared to non-exposed seronegative donors. The lytic activities of NK cells against the targets K-562 and Daudi were higher in EUs than at the controls. The proportions of NK cells producing cytokines/chimiokines were also much higher in EUs than in the controls and including in absence of any in vitro activation what suggests that NK cells from EUs were already activated in vivo. These results led us to us interested in the repertory of NK cells and the expression of the ligands of the NK cell receptor in EUs compared to Vietnamese blood donors. Our data indicate an increase in the proportion of NK cells expressing activating NK cell receptors and a reduction in the expression of inhibiting receptors in EUs compared to the controls. I started a projet concerning the role of NK in controlling HIV infection in DC. We used an in vitro model of NK/DC cross talk after HIV infection. We demonstrated that HIV infection of DC induced changes in the proliferation and NK cell repertoire in particularly an important decrease in CD85j receptor expression. We also identified a subset of NK cell expressing the CD85j receptor are able to inhibit the HIV replication in NK cells by a mechanism of cell to cell contact and none mediated by cytolytic or soluble factors. The interaction of NK cells with HIV infected DC is mediated by an unknown ligand. We are now identified the CD85j ligands (S100A family proteins) which can explain some NK dysfunctions during HIV infection. Also, we started the study of the role of NK during HIV vaccination. Our results showed 1. - MVA infection of DC leads to widespread cell death, which creates the requirement of uninfected (fresh DC) for phagocytosis and cross presentation of activating ligands from MVA-infected DC to NK cells. 2. - These dendritic cell-stimulated NK cells proliferate during 5 days in culture and distinctly alter their repertoire in response to HIV-recombinant or wild type MVA. The receptors which seem to be particularly divergent between the two MVA conditions are: CD158e, NKG2D, and NKp30. Additionally, an ‘MVA response’ was observed with all receptors tested when we compared repertoire changes after either MVA condition with uninfected media control (MVA vs DCni). 3 .- As a functional characteristic of the repertoire alterations described before, we observed that activated NK cells from the Recombinant HIV MVA condition were better at controlling HIV replication in dendritic cells in vitro as compared to wildtype MVA- or DCni-stimulated NK.
My research program is directed now towards 4 principal axes: I – Better characterization of crosstalk between dendritic and NK cells after loading DC with HIV antigens, in particular its role in the induction of VIH specific T cell responses. II – Functional studies of the functions of NK cells after stimulation of NK cell with the CD85j ligand described by us III - the study of the role of decidual NK cells in the protection of the mother to child transmission of the HIV-1 in utero (in collaboration with the group of MENU, E). IV. The study of NK cell “memory” or “priming” in patients infected with HIV and tuberculosis.