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. Author manuscript; available in PMC: 2015 Jul 9.
Published in final edited form as: Cell Host Microbe. 2014 Jul 9;16(1):19–30. doi: 10.1016/j.chom.2014.06.007

Figure 6. The VΔtail rMV is defective in MDA5 suppression and IFN antagonism in primary human DCs.

Figure 6

(A) Primary human DCs were either DMSO-treated or pre-incubated with Raf-1 inhibitor GW5074 for 2 h, and then infected with WT or VΔtail virus (MOI 0.5). Phosphorylation of endogenous MDA5 S88 (upper panel), RIG-I S8 (middle panel), and RIG-I T170 (lower panel) was determined at 8 h.p.i. (left) and 16 h.p.i. (right) by flow cytometry using phospho-specific pS88-MDA5, pS8-RIG-I and pT170-RIG-I antibodies. Data are representative of three independent donors. (B–D) DCs that had been either DMSO-treated or pre-incubated with GW5074 for 2 h, were infected with WT or VΔtail virus (MOI 0.5). IFN-β and ISG mRNA levels were determined by qRT-PCR at 24 h.p.i. Data are pooled from three (B and C) or two (D) independent donors and presented as means +/− s.d. *P<0.05; n.s., not statistically significant.