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. 2019 Oct 23;8:e49875. doi: 10.7554/eLife.49875

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© 2019, Liberatore et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 1. — (A) Schematic representation of RhIV genomes in which VSV-G ectodomain and transmembrane sequences are replaced with HIV-1 Env counterparts. (B) Western blot analysis of HIV-1 gp160/120 and VSV-M protein levels in RhIV infected cells and extracellular virions. (C) Monolayers of GHOST-X4 or GHOST-R5 cells stained with crystal violet 24 hr after infection with VSV or RhIV strains. (D) Yield of various RhIV strains in plaque forming units/ml (PFU/ml) during replication in 293 T/CD4/CCR5 cells. (E) Schematic representation of RhIV genomes in which a GFP or nanoluciferase (nLuc) reporter is included. (F,G) Micrographs of GHOST-R5 (F) and MT4-R5 (G) at the indicated times after infection with RhIV_AD17(GFP). (H) Luciferase expression in TZM-Bl cells over time following infection with RhIV_AD17(nLuc) at the indicated MOIs. (I) Inhibition of RhIV(nLuc) and corresponsing HIV-1(nLuc) strains by the CCR5 inhibitor, Maraviroc.