Figure 1.
Molecular docking model for HF with viral 3Cpro.
(A) The chemical structure for EV71 3C protein and HF. (B)Top-ranked docking conformation for HF with viral 3Cpro.
Figure 2.
Inhibition of EV71 3Cpro protease activity by FIP in vitro.
(A) Synthesis of FIP from HF by a simplified Atherton-Todd reaction. (B) Molecular docking model for FIP with viral 3Cpro. (C) Protease activity for EV71 3Cpro was noticeably inhibited by FIP (P<0.05). Standard deviations of three independent experiments are shown.
Figure 3.
Cytotoxicity test for HF and FIP on RD cells.
1–200 μM HF and FIP showed no obvious inhibitory effect on RD cell proliferation (P>0.5). The mean value was obtained from four replicate wells, and means ± SD are shown.
Figure 4.
Effects of HF and FIP on EV71 infection.
(A) Reduction of virus-induced cytopathic effects in RD cells by HF and FIP. (B) HF and FIP protected RD cells from EV71 infection (P<0.05). The experiment was performed in triplicate, and the bars represent means ± SD.
Figure 5.
Inhibition of EV71 replication by HF and FIP in RD cells.
(A) HF and FIP inhibited EV71 RNA accumulation (P<0.05). (B), (C) HF and FIP inhibited EV71 capsid protein VP1 synthesis. (D) EV71 plaque formation was reduced by addition of HF and FIP (P<0.05). The experiment was performed in triplicate, and the bars represent means ± SD.
Figure 6.
CAV10 and CBV5 replication is inhibited by HF and FIP.
Concentrations of 20 μM HF and FIP substantially inhibited replication for both CAV10 and CBV5 (P<0.05). Standard deviations of three independent experiments are shown.
Table 1.
Top-ranked docking conformation for HF and FIP with viral 3Cpro.