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Journal of Virology, March 2003, p. 3624-3633, Vol. 77, No. 6
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.6.3624-3633.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Potential Role for CD63 in CCR5-Mediated Human Immunodeficiency Virus Type 1 Infection of Macrophages

Jana J. von Lindern,1 Daniel Rojo,2 Kathie Grovit-Ferbas,3 Christine Yeramian,3 Cheng Deng,2 Georges Herbein,2 Monique R. Ferguson,2 Todd C. Pappas,2 Julie M. Decker,4 Anjali Singh,5 Ronald G. Collman,5 and William A. O'Brien1,2,6*

Departments of Microbiology and Immunology,1 Internal Medicine,2 Pathology, University of Texas Medical Branch, Galveston, Texas 77555,6 Department of Medicine, University of California at Los Angeles, the Veterans Affairs Greater Los Angeles Healthcare System,3 the UCLA AIDS Institute, Los Angeles, California 90095,4 Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 191045

Received 21 August 2002/ Accepted 20 December 2002

Macrophages and CD4+ lymphocytes are the principal target cells for human immunodeficiency virus type 1 (HIV-1) infection, but the molecular details of infection may differ between these cell types. During studies to identify cellular molecules that could be involved in macrophage infection, we observed inhibition of HIV-1 infection of macrophages by monoclonal antibody (MAb) to the tetraspan transmembrane glycoprotein CD63. Pretreatment of primary macrophages with anti-CD63 MAb, but not MAbs to other macrophage cell surface tetraspanins (CD9, CD81, and CD82), was shown to inhibit infection by several R5 and dualtropic strains, but not by X4 isolates. The block to productive infection was postfusion, as assessed by macrophage cell-cell fusion assays, but was prior to reverse transcription, as determined by quantitative PCR assay for new viral DNA formation. The inhibitory effects of anti-CD63 in primary macrophages could not be explained by changes in the levels of CD4, CCR5, or ß-chemokines. Infections of peripheral blood lymphocytes and certain cell lines were unaffected by treatment with anti-CD63, suggesting that the role of CD63 in HIV-1 infection may be specific for macrophages.

* Corresponding author. Mailing address: University of Texas Medical Branch, Division of Infectious Diseases, 301 University Blvd., Galveston, TX 77555-0435. Phone: (409) 747-2361. Fax: (409) 747-0507. E-mail: wobrien{at}utmb.edu.

Journal of Virology, March 2003, p. 3624-3633, Vol. 77, No. 6
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.6.3624-3633.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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