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Blood, 15 January 2008, Vol. 111, No. 2, pp. 699-704. Prepublished online as a Blood First Edition Paper on October 1, 2007; DOI 10.1182/blood-2007-05-088435.
IMMUNOBIOLOGY HIV-1–induced activation of CD4+ T cells creates new targets for HIV-1 infection in human lymphoid tissue ex vivo1 Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development, Bethesda, MD; and 2 Inserm UMR599, Centre de Recherche en Cancérologie de Marseille, Institut Paoli-Calmettes, Université Mediterranée, Marseille, France We demonstrate mechanisms by which HIV-1 appears to facilitate its own infection in ex vivo–infected human lymphoid tissue. In this system, HIV-1 readily infects various CD4+ T cells, but productive viral infection was supported predominantly by activated T cells expressing either CD25 or HLA-DR or both (CD25/HLA-DR) but not other activation markers: There was a strong positive correlation (r = 0.64, P = .001) between virus production and the number of CD25+/HLA-DR+ T cells. HIV-1 infection of lymphoid tissue was associated with activation of both HIV-1–infected and uninfected (bystanders) T cells. In these tissues, apoptosis was selectively increased in T cells expressing CD25/HLA-DR and p24gag but not in cells expressing either of these markers alone. In the course of HIV-1 infection, there was a significant increase in the number of activated (CD25+/HLA-DR+) T cells both infected and uninfected (bystander). By inducing T cells to express particular markers of activation that create new targets for infection, HIV-1 generates in ex vivo lymphoid tissues a vicious destructive circle of activation and infection. In vivo, such self-perpetuating cycle could contribute to HIV-1 disease.
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| Copyright © 2008 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||||
