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. Author manuscript; available in PMC: 2016 Mar 13.
Published in final edited form as: ACS Infect Dis. 2015 Jan 21;1(3):140–148. doi: 10.1021/id5000458

Figure 4.

Figure 4

Effects of helicase inhibitors on cellular flavivirus replication. (A) Subgenomic DENV replicon used in this study. (B) Percent of DENV replicon remaining in cells treated with 20 μM of each compound in the focused helicase inhibitor library plotted against the effect of 20 μM of each compound on cell viability. Dotted lines mark arbitrary cutoffs. (C) Effects of compounds in Tables 2 and 3 on DENV replicon content and cell viability (av ± SD, n = 3). (D) Effect of various concentrations of 25 on cell viability (+) and subgenomic replicon (sgR) content (○). (E) BHK cells were infected with West Nile virus in the presence of 50 μM of indicated compounds and titered 72 h later (av ± SD, n = 3). (F) Effect of various concentrations of compound 25 on West Nile virus titers (av ± SD, n = 3).