Document 0969
 DOCN  M9620969
 TI    RevM10-mediated inhibition of HIV-1 replication in chronically infected
       T cells.
 DT    9602
 AU    Escaich S; Kalfoglou C; Plavec I; Kaushal S; Mosca JD; Bohnlein E;
       Progenesys, Palo Alto, CA 94304, USA.
 SO    Hum Gene Ther. 1995 May;6(5):625-34. Unique Identifier : AIDSLINE
       MED/96078097
 AB    Two clinical regimens have been proposed for gene therapies of acquired
       immunodeficiency syndrome (AIDS): (i) Genetic modification of
       differentiated peripheral mononuclear cells ex vivo and (ii) gene
       delivery into hematopoietic stem/progenitor cells ex vivo. Various
       antiviral strategies targeted at different molecular processes in the
       human immunodeficiency virus type 1 (HIV-1) life cycle are currently
       being pursued, all with the goal of reducing HIV-1 replication. Until
       now, all successful studies have reported inhibition in acutely
       HIV-infected cells that had been genetically modified prior to
       infection. These promising results do not address a clinically relevant
       question: What is the contribution of already infected peripheral
       mononuclear and hematopoietic stem/progenitor cells to disease
       progression? In this report, we demonstrate inhibition of both HIV-1
       replication and production of infectious particles in chronically
       infected human T leukemia cell lines. The antiviral effect on the
       transduced cell population correlates with the expression of the
       dominant-negative RevM10 protein. This is the first demonstration that a
       gene therapy-based treatment can achieve antiviral efficacy in human T
       leukemia cells chronically infected with HIV-1.
 DE    Base Sequence  Cell Line  Electroporation  Gene Products, rev/*GENETICS
       *Gene Transfer  Genetic Vectors/CHEMISTRY/GENETICS  Human
       HIV-1/*PHYSIOLOGY  Leukemia Viruses, Murine/GENETICS  Leukemia, T-Cell
       Molecular Sequence Data  T-Lymphocytes/CYTOLOGY/*VIROLOGY  Tumor Cells,
       Cultured  *Virus Replication  JOURNAL ARTICLE

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