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HIV and Apoptosis: a Complex Interaction Between Cell Death and Virus Survival

  • Chapter
Viruses and Apoptosis

Part of the book series: Progress in Molecular and Subcellular Biology ((PMSB,volume 36))

Abstract

Apoptosis, or programmed cell death, is a physiological mechanism by which the cell fragments its DNA and “commits suicide” in a controlled way (Coultas and Strasser 2000). The mechanisms of apoptosis are natural and even protect against uncontrolled cellular growth as well as playing a very important role in all development systems: embryogenesis, hematopoietic differentiation and proliferation, control of tumor proliferation, and regulation of immune activation (Holtzman et al. 2000). In the particular context of the immune system, apoptosis is a highly regulated form of cell death that is essential for maintaining a constant lymphocyte population size in the face of the continuous influx of new lymphocytes and homeostatic proliferation of existing cells (Khaled and Durum 2002). In addition, it is required during an immune response to foreign antigens in order to eliminate most activated antigen-specific T-cells and thereby prevent autoimmunity (Hilderman et al. 2002). Cell death occurs through two main pathways: activation-induced cell death, which is initiated by the binding of tumour-necrosis factor family death-receptor ligands to their cognate death receptors (the extrinsic pathway), and activated T-cell autonomous death, which is mediated by Bc12-related proteins (the intrinsic pathway) and is initiated by internal sensors that transmit signals to the mitochondria (Kramer 2000; Martinou and Green 2001).

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Bermejo, M., Alcamí, J., Gil, J. (2004). HIV and Apoptosis: a Complex Interaction Between Cell Death and Virus Survival. In: Alonso, C. (eds) Viruses and Apoptosis. Progress in Molecular and Subcellular Biology, vol 36. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-74264-7_7

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