INTRODUCTION
Acquired immunodeficiency syndrome (AIDS) is a pathology caused by the retrovirus human immunodeficiency virus type 1 and type 2 (HIV-1 and HIV-2), which generally leads to the death of patients in the absence of an efficient therapy.
During the progression of the disease, HIV infection is responsible for a dramatic loss of CD4+ T lymphocytes, which are key regulators of the immune response.1-3 This decrease in the number of CD4+ T cells impairs immune system function and decreases its capacity to protect the patient from pathologies such as infection and certain cancers. Typically, HIV-1-infected cells and uninfected CD4+ T lymphocytes, also called bystander cells, die by apoptosis. This applies to the death of infected cells, bystander cells, as well as multinucleated cells, namely, the syncytia.4 More precisely, bystander cells can die either by encounter with Fas-mediated apoptosis pathways or after interaction with HIV-released proteins (gp120, Vpr, or Tat), whereas syncytia undergo a series of alterations culminating in mitotic catastrophe and cell death by apoptosis.4Recently, the characterization of the mechanism of syncytial death has experienced major advances (for review, see Castedo et al.5). Using a cellular model that reproduces the cell-to-cell fusion phenomenon, it was established that the envelope glycoprotein complex (Env)-mediated formation of syncytia involves the activation of kinases, of transcription factors (nuclear factor-B [NF-B] and p53), and of caspases; nuclear fusion; and disruption of mitochondria integrity.6-9 The main observations were reproduced in vivo in HIV-1-infected patients and ex vivo in HIV-1-infected CD4+ T lymphocytes. This enhanced knowledge of the molecular events associated with syncytial death may help us to better understand the process of the CD4+ lymphocyte depletion during AIDS progression.