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Fig. 5 | Retrovirology

Fig. 5

From: Global phosphoproteomics of CCR5-tropic HIV-1 signaling reveals reprogramming of cellular protein production pathways and identifies p70-S6K1 and MK2 as HIV-responsive kinases required for optimal infection of CD4+ T cells

Fig. 5

Effects of kinase inhibitors on HIV fusion and infection. a Gating strategy and representative fusion and infection plots in uninfected and infected primary CD4+ T cells. b Analysis of HIV fusion in the presence of PKC and PDPK1 inhibitors. Unstimulated CD4+ T cells were infected by combination reporter viruses pseudotyped with patient-derived CCR5- or CXCR4-tropic HIV Envs and bearing a β-lactamase-Vpr protein. The percentage of fusion represents the frequency of cells demonstrating cleavage of the CCF2 dye by flow cytometry 24 h after infection, normalized to no-drug controls. c Analysis of HIV infection in the presence of kinase inhibitors. Unstimulated CD4+ T cells were infected as above and LTR-driven EGFP expression monitored by flow cytometry 72 h after infection, normalized to no drug controls. d Analysis of viral post-fusion efficiency, calculated by dividing the percentage of infected cells by the percentage of fusion-positive cells. All experiments represent duplicate infections of CD4+ T cells from 3 independent healthy control subjects. *= p ≤ 0.05; **= p ≤ 0.01; ***= p ≤ 0.001

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