Document 0285
 DOCN  M9460285
 TI    Identification of CD7 glycoprotein as an accessory molecule in
       HIV-1-mediated syncytium formation and cellfree infection.
 DT    9408
 AU    Sato AI; Balamuth FB; Ugen KE; Williams WV; Weiner DB; Department of
       Pathology, University of Pennsylvania, Philadelphia; 19104.
 SO    J Immunol. 1994 May 15;152(10):5142-52. Unique Identifier : AIDSLINE
       MED/94230996
 AB    A major cytopathic effect seen upon in vitro infection of CD4+ human T
       cells by the HIV is cell-to-cell fusion that results in giant cell (or
       syncytium) formation. Membrane fusion is required for infection by
       cellfree virions and in syncytium formation. We report here that the
       human T cell surface molecule, CD7, is important for the HIV-1 fusion
       process. CD7 is a roughly 40-kDa glycoprotein member of the Ig supergene
       family that is expressed early in the ontogeny of thymocytes and on the
       majority of peripheral blood T cells, as well as on NK cells and a small
       subpopulation of B cells. Anti-CD7 mAbs inhibited HIV-1-induced
       cell-cell fusion and prevented cellfree infection of SupT1 cells. The
       antisyncytial activity of the CD7 Abs is not because of cross-reactivity
       with CD4 or with viral proteins. Epitope mapping revealed at least two
       regions of the molecule that are important for preventing membrane
       fusion. Cells rendered CD7- are poorly infectable by cellfree virus.
       Additionally, cells rendered CD7- are more easily inhibited from fusing
       in syncytium formation assays. The collective results support a central
       role for human CD7 in the process of HIV infection.
 DE    Antibodies, Monoclonal/IMMUNOLOGY  Antigenic Determinants  Antigens,
       CD/IMMUNOLOGY/*PHYSIOLOGY  Antigens, CD4/IMMUNOLOGY  Antigens,
       Differentiation, T-Lymphocyte/IMMUNOLOGY/*PHYSIOLOGY  Cell Fusion  Cell
       Line  Cross Reactions  Cytopathogenic Effect, Viral  Human
       HIV-1/*PATHOGENICITY  Support, Non-U.S. Gov't  Support, U.S. Gov't,
       P.H.S.  T-Lymphocytes/IMMUNOLOGY  JOURNAL ARTICLE

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