By George A. , Ed. Miller
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Additional resources for Cellular Aspects of HIV Infection
1996). One of the intriguing alterations in the peripheral T-cell pool of individuals infected with HIV is the progressive accumulation within the CD8 T-cell subset of a population of cells that lack expression of the CD28 costimulatory molecule. Indeed, in some HIV-infected persons, b65% of the CD8 T cells are CD28À . A more complete characterization of this unusual cell population, therefore, is essential for understanding disease pathogenesis as well as for the development of appropriate strategies for treatment.
REPLICATIVE SENESCENCE Normal human somatic cells have an intrinsic natural barrier to unlimited cell division. Following a fairly predictable number of cell divisions in culture, most, if not all, mitotically competent human cells reach an irreversible state of growth arrest known as replicative senescence, a process ®rst identi®ed by Hay¯ick in human fetal ®broblasts (Hay¯ick, 1965). Replicative senescence is a strict characteristic of human cells, and has, in fact, been proposed to constitute a tumor suppressive mechanism (Smith and Pereira-Smith, 1996).
1993). The speci®c link between telomere length and cell cycle arrest, the so-called telomere hypothesis of replicative senescence, was supported by several landmark studies published in early 1998. , 1998; Vaziri and Benchimol, 1998). , 1999). Whether similar manipulations in T cells will lead to parallel outcomes is currently being investigated in several laboratories. TELOMERE LENGTHS AND HIV DISEASE Identi®cation of the speci®c telomere sequence led to the rapid development of a variety of techniques to evaluate telomere length.
Cellular Aspects of HIV Infection by George A. , Ed. Miller