By George A. , Ed. Miller
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Extra resources for Cellular Aspects of HIV Infection
1996), and conversely, telomerase up-regulation in antigen-speci®c human T cells can be blocked by treatment of the APCs with antibodies that block the CD28/B7 interaction (Valenzuela and E¨ros, 2000b). Interestingly, antigen-speci®c T cells that are repeatedly reactivated by exposure to antigen over time in long-term culture eventually lose the ability to up-regulate telomerase and senesce in culture (Valenzuela and E¨ros, 2000b). If a similar down-regulation of telomerase inducibility occurs in vivo, this could explain the presence of CD8 T cells with shortened telomeres in situations of chronic antigenic exposure.
Kypr J, Mrazek J, Reich J. 1989. Nucleotide composition bias and CpG dinucletide content in the genomes of HIV and HTLV 1/2. Biochim Biopys Acta 1009: 280. LaBranche CC, Ho¨man TL, Romano J, Haggarty BS, Edwards TG, Matthews TJ, Doms RW, Hoxie JA. 1999. Determinants of CD4 independence for a human immunode®ciency virus type 1 variant map outside regions required for coreceptor speci®city. J Virol 73: 10310± 10319. Leigh-Brown AJ. 1991. Sequence variability of human immunode®ciency viruses: pattern and process in viral evolution.
1995), need not necessarily involve telomere shortening and, therefore, the telomere length ®ndings do not con¯ict with studies measuring repopulation, replacement, or rate of cell division. Moreover, in the absence of telomere data on speci®c CD4 T-cell subpopulations de®ned by phenotypic markers, precise conclusions from telomere studies are impossible. , 1998). , 1998). Because CD4 T cells are targets of HIV, it seems likely that those cells that become infected by HIV undergo only a few cell divisions before dying by apoptosis or being lysed by CTL, thereby limiting the time frame during which telomere shortening can occur.
Cellular Aspects of HIV Infection by George A. , Ed. Miller