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Fig. 7 | Cell & Bioscience

Fig. 7

From: Exosomes originating from infection with the cytoplasmic single-stranded RNA virus Rift Valley fever virus (RVFV) protect recipient cells by inducing RIG-I mediated IFN-B response that leads to activation of autophagy

Fig. 7

EXi-RVFV Induction of Interferon-B Is Mediated by RIG-I Activation and Is Impervious to RNase Treatment of the Exosomes. A U937 cells were transfected with RIG-I siRNA (Santa Cruz) and RIG-I expression was measured at 24 h p.i. by western blot analysis. Cells that were either left untransfected or transfected with control scrambled siRNA (Santa Cruz) were also included as controls. B U937 cells were transfected with either a scrambled control siRNA (Santa Cruz) or with RIG-I siRNA (Santa Cruz) 24 h prior to any further treatment. Subsequently, the cells were split to generate the following treatment conditions: (i) Uninfected (control); (ii) Infection with the MP12-L-V5, NSs-Flag strain of RVFV; (iii) Infection with the ΔNSs derivative of MP12 strain (positive control); (iv) Treatment with EXu without any infection; (v) Treatment with EXi-RVFV without any infection. Whole cell lysates were prepared 24 h post treatment or post infection, and analyzed by western blot for IFN-B expression. C Naïve U937 cells were either left untreated or were treated with EXu, or EXi-RVFV, or RNase-treated EXI-RVFV (EXi-RVFV + RNase), and intracellular IFN-B expression was analyzed at 24 h post treatment by western blot analysis of whole cell lysates. For each treatment condition, mean values ± SEM from three biological replicates are shown. ***P ≤ 0.005; ****P ≤ 0.0005

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