Antibody to ICAM-1 mediates enhancement of HIV-1 infection of human endothelial cells.
Human umbilical vein endothelial cells (HUVEC) can be abortively infected with HIV-1, but virus production is rescued by the addition of T cells. Monoclonal antibody (Mab) to ICAM-1, but not its Fab' fragment or MAbs to LFA-1 and PECAM-1, increases HIV-1 infection of HUVEC by enhancing HIV-1 absorption. Enhancement by anti ICAM-1 is probably due to a bridging effect different from the ADE mediated by anti-gp120 that involves FcR or CR-mediated capture of the virus-antibody complex. Since antibodies to cell membrane molecules are present in HIV-1 infected patients, the ADE mediated by such a mechanism can be important in AIDS pathogenesis.
Scheglovitova
O
O
Gamaleya Institute for Microbiology and Epidemiology, Moscow, Russia.
Scanio
V
V
Fais
S
S
Papadia
S
S
Abbate
I
I
Castilletti
C
C
Dianzani
F
F
Capobianchi
M R
MR
D000911:Antibodies, Monoclonal / Q000276:immunology*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000821:virology*; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology*; D007371:Interferon-gamma / Q000494:pharmacology
D000911:Antibodies, Monoclonal; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma