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A more recent version of this article appeared on March 1, 2007

Published online before print September 13, 2006
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0406278

Received for publication April 18, 2006.
Revised July 19, 2006.
Accepted for publication August 7, 2006.

Article

IFN-{gamma}-activated monocytes weakly produce HIV-1 but induce the recruitment of HIV-sensitive T cells and enhance the viral production by these recruited T cells

Héla Saïdi @, Giuliana Magri , Cedric Carbonneil , Nadine Nasreddine , Mary Réquena , and Laurent Bélec

Université Paris V, Unité INSERM U743 "Immunologie Humaine," Equipe "Immunité et Biothérapie Muqueuse," Centres de Recherches Biomédicales des Cordeliers, Paris, France

@ To whom correspondence should be addressed. E-mail: hela.saidi{at}u430.bhdc.jussieu.fr.


  Abstract

The ability of macrophages to adapt to changing cytokine environments results in the dominance of a particular functional phenotype of macrophages, which would play a significant role in HIV pathogenesis. In comparison with untreated macrophages (M0), we examined the role of macrophages derived from IFN-{gamma}-activated monocytes (M1) in the HIV spread. We show that M0 and M1 bind with the same efficiency as HIV-1 with a predominant role of C-type lectins in the R5-HIV attachment and of the heparan sulfate proteoglycans in the X4-HIV attachment. Despite similar levels of R5- and X4-HIV DNA, M1 replicates and weakly transmits the virus to activated T cells by releasing CXCR4- and CCR5-interacting chemokines. The blockade of dendritic cell-specific ICAM-3-grabbing nonintegrin expressed on M1 by mAb does not interfere with the viral transfer. Uninfected M1 recruits HIV-sensitive T cells efficiently and releases soluble factors, enhancing the viral production by these recruited cells. This study highlights the role of IFN-{gamma} to induce a population of macrophages that archive HIV-1 within a latent stage and cause the persistence of the virus by favoring the recruitment of T cells or enhancing the viral replication in infected CD4+ T cells.

Key Words: adsorption • infection • transfer • cytokines • chemokines






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Copyright © 2006 by the Society for Leukocyte Biology.