ENGAGEMGNT 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
Rj. Shattock et al., ENGAGEMGNT 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, The Journal of infectious diseases, 174(1), 1996, pp. 54-62
Engagement of monocytic cell membrane proteins was shown to enhance hu
man immunodeficiency virus type 1 (HIV-1) replication in monocytic cel
ls. Cross-linking of CD18, CD11a, or CD45 by immobilized antibodies pr
oduced up to an 11-fold enhancement of HIV-1 release in the OM10.1 mon
ocytic cell Line in a tumor necrosis factor-alpha (TNF-alpha)-dependen
t manner. In addition, adhesion of OM10.1 cells to immobilized interce
llular adhesion molecule-1 (ligand for CD18/CD11a) induced similar TNF
-alpha-dependent enhancement of HIV-1 replication. After phenotypic di
fferentiation of OM10.1 cells, engagement of cell membrane proteins CD
18, CD11a, CD44, CD45, or CD58 by soluble antibodies enhanced HIV-1 re
plication in a TNF-alpha-dependent manner. These data suggest that cro
ss-linkage of monocytic cell membrane proteins during cell-cell intera
ction and specifically during antigen presentation to CD4 T cells may
enhance HIV-1 replication, facilitating infection of adjacent cells.