Figure 3
Antiviral efficacy of CPMO1 and CPMO2 in HeLa cells.
(a) Quantification of CHIKV production from CPMO-treated cells by viral plaque assays. Treatment with Endo-Porter reagent (EP) and scrambled CPMOs (sCPMO1 and sCPMO2) did not interfere with CHIKV replication. CPMO1 treatment (10 μM) produced significant and sustained inhibition against CHIKV replication (M.O.I 0.1) from day 1 (p < 0.01), 2 and 3 p.i (p < 0.001), relative to mock-treated and infected cells. CPMO2 (10 μM) exhibited a lower inhibition relative to the non-treated control. (b) Western blot detection of CHIKV E2 protein (50 kDa) expression in total cell lysate of mock-treated, Endo-Porter (EP-inf), scrambled CPMO, or CPMO treated and infected cells across day 1, 2 and 3 p.i. (D1, D2, D3). (c) Quantification of relative band density of CHIKV E2 protein. (d) Western blot analysis and (e) quantification of CHIKV nsP3 protein (78 kDa) level in total cell lysate. β-actin (42 kDa) serves as loading control. Gel image presented was cropped from several original images and all gels were electrophoresed under the same conditions. Treatment of HeLa cells with CPMO1 10 μM did not produce specific inhibition against (f) Sindbis and (g) Dengue virus replication (M.O.I. 0.1 infection) when compared to the non-treated and scrambled CPMO1 controls. Error bars are indicative of mean ± s.e.m. expressed from three independent set of experiments. Statistical analysis is performed using one-way ANOVA across all groups followed by unpaired one-tailed t-test (*p < 0.05, **p < 0.001).
