Engagement of Adhesion Molecules (CD18, CD11a, CD45, CD44, and CD58) Enhances Human Immunodeficiency Virus Type 1 Replication in Monocytic Cells through a Tumor Necrosis Factor-Modulated Pathway
Open Access
- 1 July 1996
- journal article
- research article
- Published by Oxford University Press (OUP) in The Journal of Infectious Diseases
- Vol. 174 (1) , 54-62
- https://doi.org/10.1093/infdis/174.1.54
Abstract
Engagement of monocytic cell membrane proteins was shown to enhance human immunodeficiency virus type 1 (HIV-1) replication in monocytic cells. Cross-linking of CD18, CD11a, or CD45 by immobilized antibodies produced up to an 11-fold enhancement of HIV-1 release in the OM10.1 monocytic cell line in a tumor necrosis factor-α (TNF-α)-dependent manner. In addition, adhesion of OM10.1 cells to immobilized intercellular adhesion molecule-1 (ligand for CD18/CD11a) induced similar TNF-α-dependent enhancement of HIV-l replication. After phenotypic differentiation of OM10.1 cells, engagement of cell membrane proteins CD18, CD1la, CD44, CD45, or CD58 by soluble antibodies enhanced HIV-1 replication in a TNF-α-dependent manner. These data suggest that cross-linkage of monocytic cell membrane proteins during cell-cell interaction and specifically during antigen presentation to CD4 T cells may enhance HIV-1 replication, facilitating infection of adjacent cells.Keywords
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