(a) Blue edges represent physical interactions between the viral proteins and EIPs, and orange and green edges represent EIP VTP and EHF interactions to the corresponding viruses; (b) The statistical analysis of other virus-interacting EIP numbers with the corresponding interaction numbers marked in parentheses; (c) Co-localization of ATP6V0C and 3A in the co-transfected RD cells; (d) The interaction between ATP6V0C and 3A was confirmed by co-immunoprecipitation; (e) Inhibition of EV71 replication by bafilomycin A1. RD cells were infected with the EV71 virus in the presence of varying concentrations of bafilomycin A1 (0, 6.25, 12.5, 25, 50 and 100 nmol/L) for 1 h. After washing, the cells were cultured in fresh growth mediumfor an additional 12 h. The cell cultures were subjected to plaque assays. Compared with virus control, *P < 0.05, **P < 0.01, ±s, n = 3; (f) Cytotoxicity of bafilomycin A1. Percent viability of RD cells was determined normalized to the absorbance at 450 nm of a drug-free culture; (g) Inhibition of EV71 propagation by ATP6V0C siRNA; (h) Increased EV71 propagation by ATP6V0C. RD cells were transfected with ATP6V0C siRNA or pCMV-myc-ATP6V0C and subsequently infected with EV71. 24 h later, the virus RNAs in cell cultures were isolated and subjected to real time RT-PCR. Virus growth is shown as the average percentage relative to the control cells infected with EV71. *P < 0.05, ±s, n = 3.