Figure 3. DCA promotes viral replication by disrupting MAVS-mediated anti-viral immune responses.

(A) U251 cells were infected with MV-Edm (MOI = 0.2) in the presence or absence of DCA (5 mM) for 24 h, then the total RNA in cells was harvested for the determination of viral genes encoding H and N proteins by qRT-PCR (left panel), or the supernatant was harvested for determination of TCID₅₀ on Vero cells (right panel). Similar results were obtained in two independent experiments. (B) U251 cells were infected with MV-Edm (MOI = 0.2) in the presence or absence of DCA (5 mM) for 24 h, then the expression of IFNB1 and CXCL10 mRNA was determined by qRT-PCR. Means + SD of triplicates are shown. Similar results were obtained in three independent experiments. (C) U251 cells were infected with MV-Edm (MOI = 0.2) in the absence or presence of DCA (5, 10, or 20 mM) for 12 h, and supernatants were then harvested, and the protein level of IFN-β was measured by ELISA. (D) U251 cells were treated with DCA (5 mM), MV-Edm (MOI = 0.2), MV-Edm combined with DCA, or left untreated, and cultured for 24 h. Cell lysates were then harvested for immunoblotting against MAVS or pIRF3; β-actin was used as a loading control. A representative result from two independent experiments is shown. (E) U87 cells were inoculated subcutaneously into Balb/c nude mice. When tumors reached a palpable size, one group of mice received DCA (70 mg/L) in the drinking water for 10 d (n = 6). Another group was left untreated (n = 7). Then both groups of mice were injected with MV-Edm-Luc (4 × 10⁵ pfu per mouse) via tail vein. Luciferase activity was monitored by an in vivo luminescence imaging system 72 h after virus injection (left panel). Photons per cm² tumor were quantified (right panel). * p < 0.05, ** p < 0.01, *** p < 0.001.