General goal of our Unit is the dissection of the pathogenic consequences resulting from HIV infection of CD4+ T lymphocytes and macrophages. HIV perturbs the homeostatic role of the network of cytokines and chemokines whereas this latter regulates the efficiency of virus infection and propagation among immune cells by interfering at multiple levels in the virus life cycle. In this context, we are also studying the involvement of signal transduction patwhays, such as the “JAK/STAT” pathway and certain transcription factors such as NF-kB and AP-1 known to affect HIV expression. Pharmacological molecules, such as pertussis toxin and urokinase-type plasminogen activator are potent tools to unravel crucial elements of the mutual interaction between the virus and the host. In addition, they also allow the potential identification of novel agents acting either by preventing virus replication or by restoring the damaged immune system of infected individuals.