Dalgleish, A. G. et al. The role of HIV gp120 in the disruption of the immune system. Immunol. Lett. 66, 81-87
St George's, University of London, Londinium, England, United Kingdom Immunology Letters
(Impact Factor: 2.51).
04/1999; 66(1-3):81-7. DOI: 10.1016/S0165-2478(98)00163-1
The existence of HIV positive individuals who do not appear to progress to disease, or do so only very slowly (LTNPs), strongly suggest that factors other than virus pathogenicity determine disease. The occurence of HIV infected chimpanzees that remain disease free and other African SIV infected primates where disease is apparently species specific underscores the importance of host factors [1,2]. We have examined the immune response of LTNP patients using a variety of techniques including intracellular cytokine FACscan, anchor PCR analysis of the T cell receptor and HLA typing of class II genes by DNA sequencing. Our results to date confirm that the development of disease is consistent with activation of a susceptible immune system, and that this could be due to the fact that HLA-like sequences of HIV may 'allo' activate the host immune response. In order to test this hypothesis further we have examined whether gp120 itself can bind and present specific peptides which may be capable of eliciting 'allo' activation responses in particular hosts.
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ABSTRACT: We have used the erosion of telomeric DNA as a measure of cellular division to study the replicative history of isolated T-lymphocyte subpopulations from a group of HIV-infected long-term survivors and age-matched healthy controls.
In keeping with previous studies, we found that CD45RO+ (memory) T-cells showed greater telomere erosion than CD45RA+ (naive) T-cells. We did not, however, find any significant differences in the telomere lengths of isolated CD4+, CD8+, CD45RA+ or CD45RO+ T-cells between HIV-infected long-term survivors and age-matched controls. Further, we found no evidence of telomerase activation in T-cells from the HIV-infected groups to account for the lack of telomere erosion.
Our data show no evidence, through telomere shortening, of clonal exhaustion or replicative senescence due to an increased rate of immune cell turnover in HIV-infected long-term survivors.
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ABSTRACT: The emergence of HIV and AIDS is narrated here through the eyes of the legendary Irish traveller Gulliver, observing the replication, cross-species origin, evolution, diversity and transmission of HIV. Ethical problems of vaccine trials, the social impact of AIDS, and prospects for its prevention, including the development of topical virucidal lotions, are discussed. The existence of a growing proportion of HIV-infected, immunocompromised children and adults may significantly affect current immunization programmes and the evolution of opportunistic infections.
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