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J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. · Aug 1998
CD8+ T-lymphocyte activation in HIV-1 disease reflects an aspect of pathogenesis distinct from viral burden and immunodeficiency.
- Z Liu, W G Cumberland, L E Hultin, A H Kaplan, R Detels, and J V Giorgi.
- Department of Epidemiology, University of California-Los Angeles School of Public Health, 90095-1745, USA.
- J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. 1998 Aug 1; 18 (4): 332-40.
AbstractThe CD8+ T-cell response is central to control and eventual elimination of persistent viral infections. Although it might be expected that CD8+ T-cell activation would be associated with a better clinical outcome during viral infections, in long-term HIV-1 infection, high levels of CD8+ T-cell activation are instead associated with faster disease progression. In this study, cell surface expression of CD38, a flow cytometric marker of T-cell activation of CD8+ T cells, had predictive value for HIV-1 disease progression that was in part independent of the predictive value of plasma viral burden and CD4+ T-cell number. Measurements of CD38 antigen expression on CD8+ T cells in HIV-1-infected patients may be of value for assessing prognosis and the impact of therapeutic interventions. The pathogenetic reason why CD8+ T-cell activation is associated with poor outcome in HIV-1 disease remains unknown. Possibly CD8+ T-cell activation contributes to immunologic exhaustion, hyporesponsiveness of T cells to their cognate antigens, or perturbations in the T-cell receptor repertoire.
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