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CXCR4-mediated T cell apoptosis in human immunodeficiency virus infection

¹ Department of Virology and Institut d'Etude et de Transfert de Genes, University of Franche-Comte School of Medicine, Hôpital Saint-Jacques, 2 place Saint-Jacques, F-25030 Besançon cedex, France
² Department of Infectious Diseases, University of Franche-Comte School of Medicine, Hôpital Saint-Jacques, 2 place Saint-Jacques, F-25030 Besançon cedex, France

Correspondence
Georges Herbein
gherbein{at}chu-besancon.fr

Mechanisms of CXCR4-mediated T lymphocyte apoptosis in human immunodeficiency virus (HIV) infection are poorly understood. The authors used peripheral blood mononuclear cells isolated from HIV type 1-infected subjects and assessed both CD4⁺ and CD8⁺ T cell apoptosis in the presence and absence of CXCR4 blockade by AMD3100. Both CD4⁺ and CD8⁺ T cell apoptosis could be inhibited by CXCR4 blockade, mostly in acquired immunodeficiency syndrome subjects and more weakly in asymptomatic HIV-positive subjects, and depended only partially on the syncytium-inducing/non-syncytium-inducing viral envelope phenotype. Immune activation of CD8⁺, but not CD4⁺, T cells was CXCR4-dependent, resulting in increased T cell apoptosis. In the presence of monocyte-derived macrophages, CXCR4-mediated apoptosis targeted mostly CD8⁺ T cells, with CD4⁺ T cells being more weakly affected. Several immune and viral factors thus play a role in CXCR4-mediated T cell apoptosis in HIV infection: CD4/CD8 phenotype, viral envelope phenotype, T cell activation and T cell–macrophage intercellular contacts.