       Document 0551
 DOCN  M9650551
 TI    Suppression of HIV replication in human monocyte-derived macrophages
       induced by granulocyte/macrophage colony-stimulating factor.
 DT    9605
 AU    Matsuda S; Akagawa K; Honda M; Yokota Y; Takebe Y; Takemori T; AIDS
       Research Center, National Institute of Health, Tokyo, Japan.
 SO    AIDS Res Hum Retroviruses. 1995 Sep;11(9):1031-8. Unique Identifier :
       AIDSLINE MED/96089210
 AB    Susceptibility to HIV infection was examined in macrophages
       differentiated from human monocytes by macrophage colony-stimulating
       factor (M-CSF) or granulocyte/macrophage colony-stimulating factor
       (GM-CSF). The replication of macrophage-tropic human immunodeficiency
       virus type-1 (HIV-1), which was determined by reverse transcriptase (RT)
       activity, was significantly suppressed in macrophages induced by GM-CSF
       (GM-type macrophages) but not in those induced by M-CSF (M-type
       macrophages). Multinucleated giant cells were formed only in M-type
       macrophages after HIV infection. However, the expression of CD4
       molecules on the surface of both types of macrophages was similar and
       the proviral DNA was detectable in cell lysates of both macrophages,
       although the amount of proviral DNA in M-type macrophages was higher
       than that in GM-type macrophages. Many steps have been defined in HIV
       infection and replication, such as adsorption of HIV to the cell
       surface, internalization of the viral core into the cytoplasm, uncoating
       of viral RNA, reverse transcription and integration of proviral DNA into
       cellular DNA, transcription and translation of proviral DNA, assembly of
       viral components, and budding of virus particles. Our findings suggested
       that the suppression of HIV-1 replication in macrophages induced by
       GM-CSF is mainly due to a disturbance at certain steps of replication
       after synthesis of the proviral DNA. Thus, the suppression of HIV
       replication in GM-type macrophages may provide a model of the latency of
       HIV infection in vivo.
 DE    Antigens, CD4/METABOLISM  Antigens, Surface/METABOLISM  Base Sequence
       Cell Differentiation  Cells, Cultured  DNA Primers/GENETICS  DNA,
       Viral/GENETICS/METABOLISM  Genes, gag  Granulocyte-Macrophage
       Colony-Stimulating Factor/*PHARMACOLOGY  Human  HIV Infections/PATHOLOGY
       HIV-1/*DRUG EFFECTS/GENETICS/*PHYSIOLOGY  Macrophage Colony-Stimulating
       Factor/PHARMACOLOGY  Macrophages/CYTOLOGY/*DRUG EFFECTS/*VIROLOGY
       Microscopy, Electron  Molecular Sequence Data  Monocytes/CYTOLOGY/DRUG
       EFFECTS  Proviruses/DRUG EFFECTS/GENETICS/PHYSIOLOGY  Support, Non-U.S.
       Gov't  Virus Replication/*DRUG EFFECTS  JOURNAL ARTICLE

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

