Fig. 1

EV-D68 infection inhibits the expression of ADAR1. (A) RD cells were infected with EV-D68 at MOI of 0, 0.1, 0.5 and 1.0 for 24 h, and the cells were lysed for western blotting to detect the expression level of viral protein VP1 and endogenous protein ADAR1. Beta-actin was probed as the internal control. (B) ADAR1/beta-actin for each groups were calculated as described in “Materials and Methods” section. (C, D) RD cells were infected with EV-D68 at MOI of 1.0 for 0, 6, 12 and 24 h. Then the expression of viral VP1 and endogenous ADAR1 in cell lysates were detected, and ADAR1/beta-actin for each groups were calculated as described above. 293 T cells were infected with EV-D68 either at MOI of 0, 0.1, 0.5 and 1.0 for 24 h (E, F) or at MOI of 1.0 for 0, 6, 12 and 24 h (G, H). VP1 and endogenous ADAR1 were detected, and ADAR1/beta-actin were quantified as described above. (I) ADAR1 mRNA levels in RD cells from (A) were detected via RT-qPCR as described in “Materials and Methods”section. Cellular beta-actin mRNA was used as control. (J) ADAR1 mRNA levels in RD cells from (C) was detected by RT-qPCR as described above. (K, L) Hela cells were infected with HPIV3 at MOI of 0, 0.1 and 0.2 for 36 h, and the samples were collected, viral HN, endogenous ADAR1 and beta-actin were detected by western blotting. ADAR1/beta-actin for each groups were calculated as described above. In all the panels for western blotting, the relative molecular mass was marked besides each band. All data above were shown as mean ± SEM of n = 3 replicates, student’s t-test: **p < 0.01; ***p < 0.001