The human immunodeficiency virus (HIV) is the virus that causes AIDS. HIV infects key cells of our immune system: white blood cells called lymphocytes. However it is also known that another key cell of the immune system, the dendritic cell, is very important in spreading the infection inside the body. Indeed, it was found that dendritic cells can "capture" HIV without themselves getting infected. Not only do dendritic cells capture HIV, but HIV is also made more potent in subsequently infecting lymphocytes. Thus it is very important to understand both how dendritic cells capture HIV and increase its infection.
During my EMBO fellowship, I studied a molecule called "DC-SIGN" found in dendritic cell. My lab previously found that DC-SIGN could bind HIV and capture it. However this work was done in an artificial system, using cells from cancer instead of "real" dendritic cells. Thus I first studied DC-SIGN in the real cell it is found in vivo: the dendritic cell. I used a technology called "RNA interference" to remove DC-SIGN from dendritic cells. I found that even in the absence of DC-SIGN, dendritic cells are able to capture HIV fine and to increase its ability to infect lymphocytes. I documented this finding with additional experiments, describing how different forms of HIV have a totally different behavior in terms with DC-SIGN.
HIV interaction with dendritic cells is very important however still poorly understood. The work I did during my EMBO fellowship now allow us to ask two simple and important questions:
- What happens when HIV binds DC-SIGN on the dendritic cells?
- How the dendritic cell capture to increase HIV infectivity?