Journal of Leukocyte Biology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

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

Published online before print September 13, 2006
This Article
Right arrow Full Text (Reprint (PDF))
Right arrow All Versions of this Article:
jlb.0406278v1
81/3/642    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Saïdi, H.
Right arrow Articles by Bélec, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Saïdi, H.
Right arrow Articles by Bélec, L.
© 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






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2006 by the Society for Leukocyte Biology.