Fig. 1.

OAS3 inhibits EV71 replication depending on RNase L activation. 2-5A synthesis activity of OAS3 determines the inhibitory effect on EV71 replication.

A WT and inactivated mutants of OAS3 transfected HEK293T cells were infected with EV71 at an MOI of 4. The expression levels of exogenous OAS3 and VP1 were examined by Western blotting. B Viral RNA in cell lysate was examined by RT-qPCR. The RNA level of VR1012 was set as “1”. C Viral titers in the supernatants were determined by the plaque assay. D RNase L activation was examined by agarose electrophoresis of total rRNA of cells. E The negative control pLKO.1 and RNase L knockdown (RNase L KD) HEK293T cells were transfected with OAS3-expressing or control plasmids. Cells were infected with EV71 at an MOI of 4. The expression levels of endogenous RNase L, exogenous OAS3, and VP1 were examined by Western blotting. F Viral RNA in cell lysate was examined by RT-qPCR. The RNA level of VR1012 was set as “1”. G Viral titers in the supernatants were determined by the plaque assay. H RNase L activation was examined by agarose electrophoresis of total rRNA of cells. 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).