Suppression of HIV replication in human monocyte-derived macrophages induced by granulocyte/macrophage colony-stimulating factor. NLM AIDSLINE Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.

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Suppression of HIV replication in human monocyte-derived macrophages induced by granulocyte/macrophage colony-stimulating factor.

AIDS Res Hum Retroviruses. 1995 Sep;11(9):1031-8. Unique Identifier : AIDSLINE MED/96089210
Matsuda S; Akagawa K; Honda M; Yokota Y; Takebe Y; Takemori T; AIDS Research Center, National Institute of Health, Tokyo, Japan.

Abstract: 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.
Keywords: 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 ARTICLEKWDantigens,cd4/metabolismantigens,surface/metabolismbasesequencecelldifferentiationcells,cultureddnaprimers/geneticsdna,viral/genetics/metabolismgenes,gaggranulocyte-macrophagecolony-stimulatingfactor/KWDpharmacologyhumanhivinfections/pathologyhiv-1/KWDdrugeffects/genetics/KWDphysiologymacrophagecolony-stimulatingfactor/pharmacologymacrophages/cytology/KWDdrugeffects/KWDvirologymicroscopy,electronmolecularsequencedatamonocytes/cytology/drugeffectsproviruses/drugeffects/genetics/physiologysupport,non-uKWDsKWDgov'tvirusreplication/KWDdrugeffectsjournalarticle
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M9651096

Copyright © 1996 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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