Document 0034
 DOCN  M9460034
 TI    CD4 is a critical component of the receptor for human herpesvirus 7:
       interference with human immunodeficiency virus.
 DT    9408
 AU    Lusso P; Secchiero P; Crowley RW; Garzino-Demo A; Berneman ZN; Gallo RC;
       Laboratory of Tumor Cell Biology, National Cancer Institute,; National
       Institutes of Health, Bethesda, MD 20892.
 SO    Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3872-6. Unique Identifier :
       AIDSLINE MED/94224844
 AB    In this study, we demonstrate that the glycoprotein CD4, a member of the
       immunoglobulin superfamily, is a critical component of the receptor for
       human herpesvirus 7 (HHV-7), a recently discovered T-lymphotropic human
       herpesvirus. A selective and progressive downregulation of the surface
       membrane expression of CD4 was observed in human CD4+ T cells in the
       course of HHV-7 infection. Various murine monoclonal antibodies to CD4
       and the recombinant soluble form of human CD4 caused a dose-dependent
       inhibition of HHV-7 infection in primary CD4+ T lymphocytes. Moreover,
       radiolabeled HHV-7 specifically bound to cervical carcinoma cells (HeLa)
       expressing human CD4. A marked carcinoma cells (HeLa) expressing human
       CD4. A marked reciprocal interference was observed between HHV-7 and
       human immunodeficiency virus (HIV), the retrovirus that causes the
       acquired immunodeficiency syndrome and also uses CD4 as a receptor.
       Previous exposure of CD4+ T cells to HHV-7 dramatically interfered with
       infection by both primary and in vitro-passaged HIV-1 isolates.
       Reciprocally, persistent infection with HIV-1 or treatment with the
       soluble form of gp120, the CD4-binding envelope glycoprotein of HIV-1,
       rendered CD4+ T cells resistant to HHV-7 infection. These data indicate
       that CD4 is critically involved in the receptor mechanism for HHV-7. The
       antagonistic effect between HHV-7 and HIV could be exploited to devise
       therapeutic approaches to AIDS.
 DE    Antigens, CD4/*METABOLISM  Binding, Competitive  Down-Regulation
       (Physiology)  Herpesviridae Infections/*MICROBIOLOGY  Herpesvirus 7,
       Human/*METABOLISM  Human  HIV Infections/MICROBIOLOGY  HIV-1/*METABOLISM
       Receptors, Virus/*METABOLISM  Support, Non-U.S. Gov't  T4
       Lymphocytes/*MICROBIOLOGY  Viral Interference  JOURNAL ARTICLE

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