Host cell membrane proteins on human immunodeficiency virus type 1 after in vitro infection of H9 cells and blood mononuclear cells. An immuno-electron microscopic study

1 Division of Histochemistry and Electron Microscopy, Department of Pathology and Internal Medicine, University Hospital, PO Box 85.500, 3508 GA Utrecht 2 Department of Immunology, University Hospital, Utrecht 3 Human Retroviral Laboratory, Department of Medical Virology, Academic Medical Centre, Am...

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Published in:Journal of general virology Vol. 74; no. 1; pp. 129 - 135
Main Authors: Meerloo, Timo, Sheikh, Mubasher A, Bloem, Andries C, de Ronde, Anthony, Schutten, Martin, van Els, Cecile A. C, Roholl, Paul J. M, Joling, Piet, Goudsmit, Jaap, Schuurman, Henk-Jan
Format: Journal Article
Language:English
Published: Reading Soc General Microbiol 01-01-1993
Society for General Microbiology
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Summary:1 Division of Histochemistry and Electron Microscopy, Department of Pathology and Internal Medicine, University Hospital, PO Box 85.500, 3508 GA Utrecht 2 Department of Immunology, University Hospital, Utrecht 3 Human Retroviral Laboratory, Department of Medical Virology, Academic Medical Centre, Amsterdam and 4 Laboratory for Immunobiology and 5 Pathology, National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands Human immunodeficiency virus type 1 (HIV-1)-infected H9 and blood mononuclear cells (MNCs) were studied by immunogold electron microscopy for the presence of HIV-1 gag p24 protein, env gp41 and gp120 proteins, and host cell molecules CD4, CD11a, CD25, CD54, CD63, HLA class I and HLA-DR. Uninfected H9 cells and MNC membranes labelled for CD4, HLA class I and class II, and, at low density, CD11a and CD54; lysosomal structures in the cytoplasm labelled for CD63. The infected cell surface showed immunolabelling for HIV-1 proteins, as did budding particle-like structures. Immunogold labelling of the cell membrane for CD4 was almost non-existent. The level of immunolabelling for CD11a and CD54 on infected cells was greater than that on uninfected cells; this is presumably related to a state of activation during virus synthesis. Budding particle-like structures and free virions in the intercellular space were immunogold-labelled for all host cell markers investigated. This was confirmed by double immunogold labelling using combinations of HIV-1 gag p24 labelling and labelling for the respective host cell molecule. We conclude that virions generated in HIV-1-infected cells concentrate host-derived molecules on their envelope. Also molecules with a prime function in cellular adhesion concentrate on the virion. Present address: Institute of Virology, Faculty of Veterinary Medicine, University of Utrecht, The Netherlands. > Present address: Preclinical Research/Immunology, Sandoz Pharma Ltd, Basel, Switzerland. Received 29 June 1992; accepted 1 September 1992.
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ISSN:0022-1317
1465-2099
DOI:10.1099/0022-1317-74-1-129