Document 0262
 DOCN  M9550262
 TI    The prevention of cell adhesion and the cell-to-cell spread of HIV-1 in
       vitro by the alpha-glucosidase 1 inhibitor, 6-O-butanoyl castanospermine
       (MDL 28574).
 DT    9505
 AU    Bridges CG; Brennan TM; Taylor DL; McPherson M; Tyms AS; Marion Merrell
       Dow Research Institute Laboratory, MRC; Collaborative Centre, London,
       UK.
 SO    Antiviral Res. 1994 Oct;25(2):169-75. Unique Identifier : AIDSLINE
       MED/95150559
 AB    The intercellular adhesion molecule (ICAM-1, CD54) and its counter
       receptor, the integrin leukocyte function associated antigen 1 (LFA-1,
       CD11a/CD18), have important roles in the immune response. These include
       guiding leukocytes to sites of inflammation (Issekutz and Issekutz,
       1992), enhancement of antigen presentation (Moy and Brian, 1992) and
       potentiation of cytotoxic cell function (Umehara et al., 1992;
       Sanchez-Madrid et al., 1982). In addition to these activities LFA-1 and
       ICAM-1 are implicated in the cell-to-cell transmission of human
       immunodeficiency virus (HIV-1) since antibodies to CD18, CD54 or
       synthetic peptide analogs of ICAM-1 antagonise the formation of
       virus-induced syncytia (Fecondo et al., 1993; Gruber et al., 1991;
       Hildreth and Orentas, 1989; Valentin et al., 1990). The
       alpha-glucosidase 1 inhibitor 6-O-butanoyl castanospermine (MDL 28574)
       has antiviral activity for HIV which is manifested by a decrease in
       syncytia as well as the production of virus with altered gp120 and a
       reduced infectivity (Taylor et al., 1991). Previously, it has been shown
       that the alpha-glucose 1 inhibitor (MDL 28574) treatment of human
       leukocytes in vitro or mouse lymphocytes in vivo affects the detection
       of LFA-1 but not domain 1 of CD4 nor several other CD markers (Bridges
       et al., submitted for publication). Here, we demonstrate that
       pre-treatment of HIV-permissive CD4+ cells with MDL 28574 substantially
       reduces their capacity to bind with cells chronically infected with
       HIV-1 which results in reduced virus production.(ABSTRACT TRUNCATED AT
       250 WORDS)
 DE    alpha-Glucosidases/*ANTAGONISTS & INHIB  Cell Adhesion/*DRUG EFFECTS
       Cell Communication/*DRUG EFFECTS  Cell Line  Cells, Cultured
       Cytopathogenic Effect, Viral/DRUG EFFECTS  CD4-Positive
       T-Lymphocytes/CYTOLOGY/*DRUG EFFECTS/VIROLOGY  Giant Cells/DRUG EFFECTS
       Human  HIV-1/*DRUG EFFECTS/PHYSIOLOGY  Indolizines/*PHARMACOLOGY
       Intercellular Adhesion Molecule-1/PHYSIOLOGY  Lymphocyte
       Function-Associated Antigen-1/PHYSIOLOGY  JOURNAL ARTICLE

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       protected by Copyright Law (Title 17, U.S.Code).