Fig. 10

MOV10 synergistically enhances the inhibitory effect of A3G on the infectivity of HIV-1. a, b MOV10-specific siRNA was transfected in 293T cells with pcDNA3.1-A3G-HA (0.8 μg), pCMV-VSV-G (2.5 μg), and pNL4-3ΔEnv-GFP-ΔVif (7.5 μg) or pNL4-3ΔEnv-GFP (7.5 μg). 293T cells were co-transfected with pCMV-VSV-G (2.5 μg), pNL4-3ΔEnv-GFP-ΔVif (7.5 μg) or pNL4-3ΔEnv-GFP (7.5 μg), and increasing amounts of pcDNA3.1-MOV10-FLAG (0.5–1.5 μg) or pcDNA3.1-MOV10-DEAG-mutant-FLAG (0.5–1.5 μg) in the presence or absence of pcDNA3.1-A3G-HA (0.8 μg). Culture supernatants containing 5 ng of p24 were used to infect TZM-bl cells and luciferase activity was determined at 72 h post infection. For viruses with different amounts of MOV10 but no A3G, and viruses with a fixed amount of A3G combined with different amounts of MOV10 or not, the data are plotted as relative infectivity, with the control virus (pcDNA3.1) set to 100%. Error bars represent standard errors from three independent experiments. Statistical significance was determined using t test: *p ≤ 0.05; **p ≤ 0.01. c A cartoon to show the interaction between MOV10, A3G, and Vif. In the absence of MOV10, the Vif-CBF-β-Cullin 5-ElonginB-ElonginC complex is stable and triggers the proteasomal degradation of A3G. In the presence of MOV10, the assembly of Vif-CBF-β-Cullin 5-ElonginB-ElonginC complex can be disturbed by MOV10, which leads to A3G escaping from Vif-induced proteasomal degradation