Fig. 4.

OAS3 plays an important role in IFN-β1b-mediated inhibition of EV71. A IFN-β treatment induces the expression of OAS in HEK293T cells. HEK293T cells were treated with 250 U/mL IFN-β1b, 250 U/mL IFN-γ, and 250 U/mL IL-29 for 48 ​h, and the expression levels of OAS3 were examined by RT-qPCR at different time points. The RNA level of “0 ​h” was set as “1”. B HEK293T shRNA control (pLKO.1) and shOAS3 cells were pretreated with or without 250 U/mL IFN-β for 24 ​h prior to EV71 infection at MOIs of 2 and 4. Apparent CPE was observed at 48 ​h.p.i. C Cell viability in the experiment of Fig. 4B was measured by CCK8. D The expression levels of VP1 were examined by Western blotting. E The expression levels of EV71 viral RNA were examined by RT-qPCR. The RNA level at an MOI of 0 was set as “1”. F Viral titers in the supernatants were determined by the plaque assay. The results represent the means ​± ​standard deviation from three independent experiments. Statistical significance was analyzed using Student's t-test (# no significance, ∗∗P ​< ​0.01).