The major interest of our lab is the understanding of the specific immunity mounted following pathogen infection, with a particular focus on HIV. Our goal is to define correlates of protective immunity against HIV infection. The identification of cellular immune parameters important for virus control will help us to design vaccines able to control HIV infection and eventually to prevent or cure HIV infection.
Previous studies in our lab and others show that CD8 T-cells are a major player in the control of HIV infection. We therefore try to better understand their role at the molecular level as well as at the cellular level.
During HIV infection, the virus infects and replicates primarily in CD4 T-cells. Patients that are infected receive an anti retroviral treatment (ART) which suppresses virus replication below the limit of detection for routine HIV-RNA assays. However if treatment is interrupted, viremia is rapidly detected again indicating that ART does not eliminate the virus. Understanding where and how the virus persists is therefore critical for the design of targeted therapeutics which may ultimately eradicate the virus.
Although an immune response is generated following HIV infection, it is not able to control the virus over the long term. One of the reasons behind this lack of control is the ability of the virus to rapidly evolve and change its surface protein gp120. We therefore strive to better understand the mechanisms behind the capacity of HIVgp120 to mutate and escape immune control.