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Lookup NU author(s): Dr Christopher DuncanORCiD
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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.
Author(s): Baxter AE, Russell RA, Duncan CJ, Moore MD, Willberg CB, Pablos JL, Finzi A, Kaufmann DE, Ochsenbauer C, Kappes JC, Groot F, Sattentau QJ
Publication type: Article
Publication status: Published
Journal: Cell Host and Microbe
Print publication date: 10/12/2014
Online publication date: 20/11/2014
Acceptance date: 14/10/2014
ISSN (print): 1931-3128
ISSN (electronic): 1934-6069
Publisher: Cell Press
PubMed id: 25467409
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