J Virol, August 1998, p. 6671-6677, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Institute for Hygiene1
and
Department of Ear,
Received 16 January 1998/Accepted 9 April 1998
Previous studies have shown that human immunodeficiency virus type
1 (HIV-1) exploits dendritic cells (DC) to replicate and spread among
CD4+ T cells. To explain the predominance of
non-syncytium-inducing (NSI) over syncytium-inducing (SI) strains
during the initial viremia of HIV, we investigated the ability of blood
monocyte (Mo)-derived DC to transmit HIV-1 to CD4+ cells of
the monocytoid lineage. First, we demonstrate that in our system, DC
are able to transmit NSI strains, but not SI strains, of HIV-1 to fresh
blood Mo and to Mo-derived macrophages (MDM). To establish a
productive infection, a 10-fold-lower amount of virus was necessary for
DC-mediated transmission of HIV-1 to Mo than in case of cell-free
infection. Second, immature CD83
DC (imDC) transmit virus
to Mo and MDM with higher efficacy compared to mature CD83+
DC (maDC); this finding is in contrast to data previously obtained with
CD4+ T cells. Third, maturation from imDC to maDC
efficiently silenced expression of
2-integrins CD11b,
CD11c, and CD18 by maDC. Moreover, monoclonal antibody against CD18
inhibited transmission of HIV-1 from imDC to Mo. We propose that the
adhesion molecules of the CD11/CD18 family, involved in cell-cell
interactions of DC with the microenvironment, may play a major role in
imDC-mediated HIV-1 infection of Mo and MDM.
*
Corresponding author. Mailing address: Institut
für Hygiene, Fritz-Pregl-Str. 3, Leopold-Franzens-Universität, 6020 Innsbruck, Austria. Phone:
43-512-507-3422. Fax: 43-512-507-2870. E-mail: Laco.Kacani{at}uibk.ac.at.
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