Abstract
Acquired immunodeficiency syndrome (AIDS) is a complex disease process induced by human immunodeficiency virus (HIV-1) infection.1 Although the linkage between HIV-1 infection and the development of AIDS has been established for a decade, 2 the molecular and biochemical basis for the profound and irreversible depletion of helper CD4+ T cells that follows HIV infection and paralyzes the immune system is not understood. A number of mechanisms have been proposed to account for CD4+ T killing by HIV, including the direct lysis of virally-infected cells, and the functional disruption of uninfected cells through an interaction with viral proteins.1,3,4 A recent hypothesis has proposed that, in HIV-infected individuals, there reemerges a cell death program normally utilized by immature T cells during development in response to specific stimuli accounting for both the early qualitative and late quantitative CD4+ T cell defects associated with AIDS.5
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Tian, H. et al. (1994). Cells Undergoing HIV Envelope-Mediated Programmed Degeneration Accumulate in G2/M Phase. In: Hu, V.W. (eds) The Cell Cycle. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2421-2_42
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DOI: https://doi.org/10.1007/978-1-4615-2421-2_42
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