Fig. 5. MOV10 activates innate immune signaling independent of RIG-I-MAVS.

(A) Inhibition of SeV replication by MOV10 in both MAVS-KO and RIG-I-KO 293T cells. MAVS and RIG-I-deficient 293T along with control 293T cells were infected with SeV (50 HAU/ml) for 48 h followed by SeV-specific RNA detection by qRT-PCR.

(B) Enhanced IFNβ induction by MOV10 in 293T-MAVS-KO cells. Cells were transfected either with vector or MOV10 as indicated, followed by SeV (240 HAU/ml) infection for 24 h. IFNβ protein levels in the culture supernatants were assayed as before.

(C) Silencing of MOV10 and RIG-I shows additive enhancement of VSV replication in fibroblasts. Human primary foreskin fibroblasts were transfected with indicated siRNA for 72 h and subsequently infected with VSV (0.1 m.o.i) for 16 h (F). Viral replication was quantitated by GFP-fluorescence as before (Fig. 2A). Representative micrographs are shown in Fig. S3B.

(D–E) Loss of MOV10 further enhances VSV replication in RIG-I-deficient cells. Lysates from 293T-RIG-I-KO, 293T-MOV10-KO/RIG-I-KO and 293T-MOV10-KO cells were analyzed by immunoblotting with indicated antibodies (D). Indicated cells were infected with VSV (0.1 m.o.i.) and VSV RNA analyzed by qRT-PCR 16 h post-infection (G). Plots show mean with standard error bars, where * and ** are P < 0.05 and P < 0.01 respectively by two-tailed Student’s t test analysis, and was set as 1 for comparison.