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.
basic_science · Level V
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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-alpha (TNF-alpha)-dependent manner. In addition, adhesion of OM10.1 cells to immobilized intercellular adhesion molecule-1 (ligand for CD18/CD11a) induced similar TNF-alpha-dependent enhancement of HIV-1 replication. After phenotypic differentiation of OM10.1 cells, engagement of cell membrane proteins CD18, CD11a, CD44, CD45, or CD58 by soluble antibodies enhanced HIV-1 replication in a TNF-alpha-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.
Medical subject headings
- Antigens, CD
- Cell Adhesion Molecules
- HIV-1
- Monocytes
- Tumor Necrosis Factor-alpha
- Virus Replication