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

Gorry PR, Francella N, Lewin SR, Collman RG

  • Journal Journal of leukocyte biology

  • Published 24 Oct 2013

  • Volume 95

  • ISSUE 1

  • Pagination 71-81

  • DOI 10.1189/jlb.0713368


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.