Fig. 2
FAC inhibited HIV, ZIKV and EV71 infections. a Human PBMC-differentiated dendritic cells were infected with HIV-1 (Gag/p24 100 ng/ml) ± FAC (100 μM). 8, 24, 48, and 72 h later, HIV Gag RNA loading was analyzed through real-time PCR. b Vero cells were infected with ZIKV (MOI = 0.01) ± FAC (100 μM). Seventy two-hour later, viral titers in supernatants were analyzed. c U251 cells were infected with Zika virus (MOI = 0.1) ± FAC (100 μM). 24, 48 and 72 h later, viral RNA loading was analyzed through real-time PCR. d–f RD cells were infected with EV71 (MOI = 0.1) ± FAC (100 μM) for 8 h. Viral RNA loading was detected via real-time PCR (d). Cytopathy images were captured through bright field microscopy (e). Scale bars, 100 μm. Viral VP1 protein expression was detected via western blot (f). g RD cells were infected with EV71 (MOI = 0.1) and treated with increasing doses of FAC (μM). 1 h later, viruses were washed out and FAC was supplemented. 9 h later, viral titers in supernatant were analyzed through TCID50 method. h, i 6–8-week old female IFNRα/β−/−IFNγ−/− mice were intraperitoneally infected with 40 PFU ZIKV diluted in 800 μl PBS or PBS with FAC (15 mM) (each group, n = 5). Mice weight change (h) and survival rate (i) were recorded. P < 0.0001 in (h) (PBS versus FAC, 2-way ANOVA test). P < 0.05 in (i) (PBS versus FAC, log-rank (Mantel-Cox) test). Data are representative of at least two independent experiments in (a–g). Error bars represent SEM in (h) or SD in other panels
