PII: S0167-5699(99)01471-1 cells from human immunodeficiency virus type 1 (HIV-1)infected individuals are particularly susceptible to cell death. This occurs when cells are cultured without mitogenic stimuli, but is markedly increased after stimulation through the T-cell receptor (TCR). A number of explanations have been proposed to account for these phenomena, including interactions between virus/viral proteins and TCR/CD4 molecules, lack of appropriate costimulary signals and dysregulation of death regulatory proteins (such as Bcl2 and CD95) [1][2][3][4][5][6][7] .
Apoptotic and necrotic mechanisms of cell death coexist in HIV infection
It is commonly believed that cell death occurs from apoptosis, but in reality there are multiple pathways leading to cell death in T cells from HIV-1-infected individuals, and a substantial proportion of T-cell mortality does not appear to occur via classical apoptosis. Apoptotic cells are certainly observed after culture of T cells in the absence of interleukin-2 (IL-2), due to growth factor withdrawal or CD95-CD95 ligand (CD95L) interactions [3][4][5] . Nevertheless, mitogenically stimulated cells do not appear to die by this mechanism [8][9][10][11] . In this article we describe a novel mechanism of activation-induced cell death, that has many features of necrosis [8][9][10][11] , a phenomenon referred to as activation-associated necrosis (AAN).