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.
Gorry, P. R., Francella, N., Lewin, S. R., & Collman, R. G. (2014). HIV-1 envelope-receptor interactions required for macrophage infection and implications for current HIV-1 cure strategies. Journal of leukocyte biology, 95(1), 71 - 81. https://doi.org/10.1189/jlb.0713368