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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.

Original publication

DOI

10.1016/j.chom.2014.10.010

Type

Journal article

Journal

Cell Host Microbe

Publication Date

10/12/2014

Volume

16

Pages

711 - 721

Keywords

CD4-Positive T-Lymphocytes, Cell Line, HIV Infections, HIV-1, Humans, Macrophages, Receptors, HIV, Viral Envelope Proteins, Viral Tropism