ABSTRACT
Th e immune system can use several strategies to fi ght viral infections. Among these, the death of infected cells has ultimately the role of avoiding the spread of infection, even if in most cases either the cells containing the virus or ‘innocent’ cells are killed. Th us, in diff erent situations, as defence mechanisms, every living organism can trigger apoptosis, autophagy and eventually necrosis. In turn, viruses are able to evade the immune response by interfering with several mechanisms and components. Th e human immunodefi ciency virus (HIV), that causes the acquired immunodefi ciency syndrome (AIDS), infects a huge number of cells expressing the CD4 molecule, including monocytes and T helper lymphocytes, that can trigger apoptosis. HIV encodes proteins with pro-apoptotic activity, such as gp120, gp160, Tat, Nef, Vpr, Vpu, Vif and the viral protease. Th ese proteins can provoke the death of infected and uninfected lymphocytes through several mechanisms, including the action of host-encoded molecules belonging to the tumor necrosis factor (TNF) family, or via the mitochondrial apoptotic pathway. Th e acute and chronic phases of HIV infection are characterized by a proinfl ammatory status that facilitates cell death, and is a further cause of immune damage. Nowadays the therapy for HIV/AIDS includes potent antiretroviral drugs, that are able to decrease apoptosis by diff erent mechanisms. Indeed, not only drugs diminish the production of the virus by infected cells, and thus reduce the infl ammation and the production of apoptogenic molecules, but also have a direct
action on the viral protease. Finally, the host’s genetic background plays a main role in the entire process of cell death in HIV infection.
