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Science 2 June 1989:
Vol. 244. no. 4908, pp. 1075 - 1078
DOI: 10.1126/science.2543075
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Articles

Science, Vol 244, Issue 4908, 1075-1078
Copyright © 1989 by American Association for the Advancement of Science

articles

Involvement of a leukocyte adhesion receptor (LFA-1) in HIV-induced syncytium formation

JE Hildreth and RJ Orentas

Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205.

Cell fusion (syncytium formation) is a major cytopathic effect of infection by human immunodeficiency virus (HIV) and may also represent an important mechanism of CD4+ T-cell depletion in individuals infected with HIV. Syncytium formation requires the interaction of CD4 on the surface of uninfected cells with HIV envelope glycoprotein gp120 expressed on HIV-infected cells. However, several observations suggest that molecules other than CD4 play a role in HIV-induced cell fusion. The leukocyte adhesion receptor LFA-1 is involved in a broad range of leukocyte interactions mediated by diverse receptor-ligand systems including CD4-class II major histocompatibility complex (MHC) molecules. Possible mimicry of class II MHC molecules by gp120 in its interaction with CD4 prompted an examination of the role of LFA-1 in HIV-induced cell fusion. A monoclonal antibody against LFA-1 completely inhibited HIV-induced syncytium formation. The antibody did not block binding of gp120 to CD4. This demonstrates that a molecule other than CD4 is also involved in cell fusion mediated by HIV.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Human Immunodeficiency Virus Type 1 Replication in Dendritic Cell-T-Cell Cocultures Is Increased upon Incorporation of Host LFA-1 due to Higher Levels of Virus Production in Immature Dendritic Cells.
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Cutting Edge: Productive HIV-1 Infection of Dendritic Cells via Complement Receptor Type 3 (CR3, CD11b/CD18).
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Treatment with Anti-LFA-1 Delays the CD8+ Cytotoxic-T-Lymphocyte Response and Viral Clearance in Mice with Primary Respiratory Syncytial Virus Infection.
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Endocytosis Is a Critical Step in Entry of Subgroup B Avian Leukosis Viruses.
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Unique Monoclonal Antibody Recognizing the Third Extracellular Loop of CXCR4 Induces Lymphocyte Agglutination and Enhances Human Immunodeficiency Virus Type 1-Mediated Syncytium Formation and Productive Infection.
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Muramyl dipeptide and mononuclear cell supernatant induce Langhans-type cells from human monocytes.
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LFA-1 Expression on Target Cells Promotes Human Immunodeficiency Virus Type 1 Infection and Transmission.
C. E. Hioe, P. C. Chien Jr., C. Lu, T. A. Springer, X.-H. Wang, J. Bandres, and M. Tuen (2001)
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S. Y. Chan, R. F. Speck, M. C. Ma, and M. A. Goldsmith (2000)
J. Virol. 74, 4933-4937
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Evidence for Budding of Human Immunodeficiency Virus Type 1 Selectively from Glycolipid-Enriched Membrane Lipid Rafts.
D. H. Nguyen and J. E. K. Hildreth (2000)
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Retrovirus receptors.
M. A. Sommerfelt (1999)
J. Gen. Virol. 80, 3049-3064
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Syncytium-Inhibiting Monoclonal Antibodies Produced against Human T-Cell Lymphotropic Virus Type 1-Infected Cells Recognize Class II Major Histocompatibility Complex Molecules and Block by Protein Crowding.
J. E. K. Hildreth (1998)
J. Virol. 72, 9544-9552
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CD44 Occupancy Prevents Macrophage Multinucleation.
H. Sterling, C. Saginario, and A. Vignery (1998)
J. Cell Biol. 143, 837-847
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MFR, a Putative Receptor Mediating the Fusion of Macrophages.
C. Saginario, H. Sterling, C. Beckers, R. Kobayashi, M. Solimena, E. Ullu, and A. Vignery (1998)
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Modulation of Human Immunodeficiency Virus Type 1-Induced Syncytium Formation by the Conformational State of LFA-1 Determined by a New Luciferase-Based Syncytium Quantitative Assay.
B. Barbeau, J.-F. Fortin, N. Genois, and M. J. Tremblay (1998)
J. Virol. 72, 7125-7136
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T Cells Expressing Activated LFA-1 Are More Susceptible to Infection with Human Immunodeficiency Virus Type 1 Particles Bearing Host-Encoded ICAM-1.
J.-F. Fortin, R. Cantin, and M. J. Tremblay (1998)
J. Virol. 72, 2105-2112
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Pseudopeptide TASP Inhibitors of HIV Entry Bind Specifically to a 95-kDa Cell Surface Protein.
C. Callebaut, E. Jacotot, B. Krust, G. Guichard, J. Blanco, A. Valenzuela, J. Svab, S. Muller, J.-P. Briand, and A. G. Hovanessian (1997)
J. Biol. Chem. 272, 7159-7166
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The Immunopathogenesis of Human Immunodeficiency Virus Infection.
G. Pantaleo, C. Graziosi, and A. S. Fauci (1993)
N. Engl. J. Med. 328, 327-335
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Participation of tyrosine phosphorylation in the cytopathic effect of human immunodeficiency virus-1.
D. Cohen, Y Tani, H Tian, E Boone, L. Samelson, and H. Lane (1992)
Science 256, 542-545
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The ability of certain SIV vaccines to provoke reactions against normal cells.
A. Langlois, K. Weinhold, T. Matthews, M. Greenberg, and D. Bolognesi (1992)
Science 255, 292-293
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