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. Author manuscript; available in PMC: 2024 Aug 22.
Published in final edited form as: Cell Rep. 2024 Jun 28;43(7):114414. doi: 10.1016/j.celrep.2024.114414

Figure 5. mTOR inhibition counteracts the effect of ATRA on CCR5 expression and HIV replication and integration.

Figure 5.

MDMs generated as in Figure 1A were treated with the mTOR inhibitor INK128 (50 nM) 2 days before infection and the day of infection.

(A) The representative flow cytometry histograms of extracellular CD4, CCR5, and CXCR4 expressions.

(B) Statistical analyses of the relative MFI of CD4, CCR5, and CXCR4 expressions.

(C and D) A fraction of MDMs, pretreated or not with INK128, were exposed to T/F HIVTHRO. Cells and cell-culture supernatants were harvested on day 3 post infection for the quantification of integrated HIV-DNA by nested real-time PCR (C) and soluble HIV-p24 by ELISA (D).

(E and F) In parallel, another fraction of ATRA-MDMs and DMSO-MDMs pretreated with INK128 were exposed to HIVVSV-G for 3 days. Shown are the levels of early reverse transcripts (RU5; E, left panel), late reverse transcripts (Gag; E, center panel), integrated HIV-DNA (Alu; E, right panel), as well as the levels of HIV-p24 (F). Experiments were performed on MDMs from n = 8 HIV-uninfected individuals. Repeated measures (RM) one-way ANOVA, Tukey’s test, and Wilcoxon p values are indicated on the graphs.