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Updated: Sep 27, 2026
Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
Potential role for CD63 in CCR5-mediated human immunodeficiency virus type 1 infection of macrophages
Jana J von Lindern1, Daniel Rojo, Kathie Grovit-Ferbas
1Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77555, USA.
Abstract:
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 beta-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.
Insights
Monoclonal antibody targeting CD63 inhibits human immunodeficiency virus type 1 (HIV-1) infection in macrophages. This inhibition occurs post-fusion but before reverse transcription, suggesting a specific role for CD63 in macrophage tropism.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Macrophages and CD4(+) lymphocytes are primary targets for HIV-1.
- Molecular mechanisms of HIV-1 infection can differ between cell types.
- Identifying cellular molecules involved in macrophage infection is crucial.
Purpose of the Study:
- To identify cellular molecules involved in HIV-1 infection of macrophages.
- To investigate the role of CD63 in HIV-1 macrophage tropism.
- To determine the stage of viral replication affected by CD63.
Main Methods:
- Utilized monoclonal antibodies (MAbs) against tetraspanins, including CD63.
- Assessed HIV-1 infection inhibition in primary macrophages.
- Performed cell-cell fusion assays and quantitative PCR for viral DNA.
- Analyzed changes in CD4, CCR5, and beta-chemokine levels.
Main Results:
- Anti-CD63 MAb inhibited infection by R5 and dualtropic HIV-1 strains in macrophages.
- Inhibition was post-fusion but prior to reverse transcription.
- Other tetraspanin MAbs (anti-CD9, -CD81, -CD82) did not inhibit infection.
- Anti-CD63 did not affect infection of lymphocytes or other cell lines.
Conclusions:
- CD63 plays a specific role in HIV-1 infection of macrophages.
- The inhibitory mechanism involves a post-fusion, pre-reverse transcription step.
- CD63's role in HIV-1 infection appears to be macrophage-specific.
