Document 0255
 DOCN  M95A0255
 TI    Antibody to ICAM-1 mediates enhancement of HIV-1 infection of human
       endothelial cells.
 DT    9510
 AU    Scheglovitova O; Scanio V; Fais S; Papadia S; Abbate I; Castilletti C;
       Dianzani F; Capobianchi MR; Gamaleya Institute for Microbiology and
       Epidemiology, Moscow,; Russia.
 SO    Arch Virol. 1995;140(5):951-8. Unique Identifier : AIDSLINE MED/95328955
 AB    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.
 DE    Antibodies, Monoclonal/*IMMUNOLOGY  Cells, Cultured  Endothelium,
       Vascular/*VIROLOGY  Human  HIV-1/*PHYSIOLOGY  Intercellular Adhesion
       Molecule-1/*PHYSIOLOGY  Interferon Type II/PHARMACOLOGY  Support,
       Non-U.S. Gov't  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).