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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: Antiviral Res. 2015 Jun 15;120:134–139. doi: 10.1016/j.antiviral.2015.06.006

Fig. 4. Dose-dependent inhibition of HEV replication by PPMO.

Fig. 4

A. Luciferase assay of S10-3 cells transfected with Sar55 RNA from HEV replicon pSK-E2-Luc. Cells were transfected with the viral RNA, treated with 16 μM PPMO 5 h later, and harvested for luciferase assay at 7 days post-transfection. Relative percentages of luciferase activity are shown in comparison with mock-treated S10-3 cells. Error bars represent standard errors among three repeat experiments. ** indicates significant difference from the mock-treated cells (P < 0.01). B. Dose-dependent inhibition of HEV replication by PPMO, using the same experimental scheme as in A above. C. Treatment of S10-3 cells with PPMO HP1 inhibits HEV capsid protein production in a dose-dependent manner. Cells were transfected with HEV RNA from pSK-E2, treated with PPMO HP1 5 h later and harvested 7 days later for Western blotting. A representative blot of three independent experiments is shown. D. HEV RNA levels present in supernatant of S10-3 cells treated with PPMO. Cells were transfected with Sar55 RNA and treated 8 μM PPMO HP1 5 h later. The cell culture supernatant was harvested 7 days post-transfection and RNA detected by RT-qPCR. The result shows average of four repeat treatments.