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Updated: Apr 20, 2026
Phagosome Migration and Velocity Measured in Live Primary Human Macrophages Infected with HIV-1
Published on: September 5, 2016
Macrophage infection via selective capture of HIV-1-infected CD4+ T cells
Amy E Baxter1, Rebecca A Russell2, Christopher J A Duncan2
1The Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK; Department of Medicine, Université de Montréal, Montreal, Quebec, H2X 0A9, Canada; Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Université de Montréal, Montreal, Quebec, H2X 0A9, Canada.
Abstract:
Macrophages contribute to HIV-1 pathogenesis by forming a viral reservoir and mediating neurological disorders. Cell-free HIV-1 infection of macrophages is inefficient, in part due to low plasma membrane expression of viral entry receptors. We find that macrophages selectively capture and engulf HIV-1-infected CD4+ T cells leading to efficient macrophage infection. Infected T cells, both healthy and dead or dying, were taken up through viral envelope glycoprotein-receptor-independent interactions, implying a mechanism distinct from conventional virological synapse formation. Macrophages infected by this cell-to-cell route were highly permissive for both CCR5-using macrophage-tropic and otherwise weakly macrophage-tropic transmitted/founder viruses but restrictive for nonmacrophage-tropic CXCR4-using virus. These results have implications for establishment of the macrophage reservoir and HIV-1 dissemination in vivo.
Insights
Macrophages efficiently infect HIV-1 by engulfing infected T cells, bypassing typical entry barriers. This cell-to-cell transmission establishes viral reservoirs and impacts disease progression.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Macrophages play a key role in HIV-1 pathogenesis, contributing to viral reservoirs and neurological damage.
- Cell-free HIV-1 infection of macrophages is limited by low expression of viral entry receptors on their surface.
Purpose of the Study:
- To investigate the mechanism of HIV-1 infection in macrophages.
- To understand how macrophages become infected with HIV-1 despite low receptor expression.
Main Methods:
- Observational study of macrophage-T cell interactions.
- Analysis of viral entry pathways and permissiveness to different HIV-1 strains.
Main Results:
- Macrophages selectively engulf HIV-1-infected CD4+ T cells, leading to efficient infection.
- This cell-to-cell uptake is independent of viral envelope glycoproteins and T cell receptor interactions.
- Macrophages infected via this route are permissive to macrophage-tropic HIV-1 strains but not CXCR4-using strains.
Conclusions:
- Cell-to-cell transfer from infected T cells is a primary route for macrophage infection with HIV-1.
- This mechanism contributes to the establishment of macrophage viral reservoirs and HIV-1 dissemination.
- Understanding this pathway offers new insights into HIV-1 pathogenesis and potential therapeutic targets.
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