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J Leukoc Biol. 2014 Jan;95(1):71-81. doi: 10.1189/jlb.0713368. Epub 2013 Oct 24.

HIV-1 envelope-receptor interactions required for macrophage infection and implications for current HIV-1 cure strategies.

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1.GPO Box 2284, Melbourne 3001, Victoria, Australia. or University of Pennsylvania, 522 Johnson Pavilion, 36th and Hamilton Walk, Philadelphia, PA 19104-6060, USA. E-mail:


Myeloid cells residing in the CNS and lymphoid tissues are targets for productive HIV-1 replication, and their infection contributes to the pathological manifestations of HIV-1 infection. The Envs can adopt altered configurations to overcome entry restrictions in macrophages via a more efficient and/or altered mechanism of engagement with cellular receptors. This review highlights evidence supporting an important role for macrophages in HIV-1 pathogenesis and persistence, which need to be considered for strategies aimed at achieving a functional or sterilizing cure. We also highlight that the molecular mechanisms underlying HIV-1 tropism for macrophages are complex, involving enhanced and/or altered interactions with CD4, CCR5, and/or CXCR4, and that the nature of these interactions may depend on the anatomical location of the virus.


CCR5; CD4; CXCR4; reservoir

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