Document 3290
 DOCN  M94A3290
 TI    HIV infection of adherent cells and expression of membrane molecules.
 DT    9412
 AU    Dolei A; Serra C; Tilocca F; Ceraulo F; Conaldi PG; Modesti A; Ameglio
       F; Toniolo A; Inst. of Microbiology & Virology, Univ. of Sassari, Italy.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):11 (abstract no. 017A). Unique
       Identifier : AIDSLINE ICA10/94369285
 AB    OBJECTIVE: Human cells of mesenchymal and epithelial origin were
       analyzed with respect to plasmamembrane molecules and sensitivity to HIV
       adsorption and replication. METHODS: By the use of a panel of monoclonal
       antibodies, we evaluated the expression and modulation by HIV infection,
       of molecules involved in HIV adsorption, such as CD4, galactocerebroside
       (GalC) and CD26, and molecules that can contribute to HIV unspecific
       binding to cells, such as HLA Class I and II and several adhesion
       molecules (VCAM, ICAM, ELAM, CD44, CD49d, etc.). HIV-1 adsorption and
       replication (intra- and extracellular virus) was evaluated as ability to
       form syncytia in the C8166 T cell line, and as production of p24 antigen
       in ELISA. RESULTS: HIV-1 binds to and replicates in all the cells
       tested. CD4 expression was detected in normal fibroblasts from lung,
       breast and gingiva, and, as expected, in HeLa-T4 cells. GalC was
       detected in mammary epithelial MEC-2 cells and in HeLa-T4, and, to a
       lesser extent, on normal fibroblasts; rhabdomyosarcoma and endothelial
       cells were GalC-negative. CD26 was found on all the cells. It was not
       possible to correlate CD26 expression on cells to HIV binding
       capability, or to syncytia formation. However, CD26 expression was
       stimulated in HIV-infected cells. In addition, HIV infection of
       DR-negative MEC-2 cells induced the expression of DR, and modulated that
       of some adhesion molecules. It remains to clarify whether the effects
       observed in infected cells are due to HIV per se or they are mediated by
       some of the cytokines induced by HIV in adherent cells, such as IL-6,
       TNF alpha and IL-1 beta, that have been found to increase CD4 expression
       and HIV adsorption in fibroblasts and HeLa-T4 cells (Dolei et al., Arch
       Virol 134:157, 1994). HIV infection of MEC-2 cells downregulated the
       expression of some markers of mammary differentiation, such as EMA
       (epithelial membrane antigen) and HMFG1 (human milk fat globulel). This
       was in keeping with the reduction of lipid vacuoles formation observed
       in infected monolayers scored under the microscope.
 DE    Adsorption  Antigens, CD4/METABOLISM  Antigens, Differentiation,
       T-Lymphocyte/METABOLISM  Cell Adhesion Molecules/METABOLISM  Cells,
       Cultured  Galactosylceramides/METABOLISM  Human  HIV Core Protein
       p24/BIOSYNTHESIS  HIV Infections/*IMMUNOLOGY/MICROBIOLOGY  HIV-1/GROWTH
       & DEVELOPMENT  HLA Antigens/METABOLISM  Support, Non-U.S. Gov't  Virus
       Replication  MEETING ABSTRACT

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