FIG 7.

IL-1β triggers p53-mediated inhibition of CCR5-dependent HIV-1 entry in macrophages through miR-103. MDMs derived from different blood donors (n = 3) were treated with the indicated reagents for 48 h and then left untreated or additionally treated with miR-103 antagomirs. (A) Macrophages were then infected with either the VSV-G- or HIV-Env (ADA)-pseudotyped Blam-Vpr-containing viruses. Bars represent mean viral fusion efficiencies compared to VSV-G-pseudotyped virus fusion in control-treated cells (“fusion index”). Statistics were calculated by Wilcoxon matched-pairs signed-rank tests. (B) Data from a representative experiment (numbers represent percentages of Alexa Fluor 405-positive cells). N.I., noninfected control.