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. Author manuscript; available in PMC: 2011 Nov 18.
Published in final edited form as: Cell Host Microbe. 2010 Nov 18;8(5):422–432. doi: 10.1016/j.chom.2010.10.006

Figure 7. Defects in DENV replication caused by autophagy inhibition can be complimented by exogenous free fatty acids.

Figure 7

(A) Huh-7.5 cells were electroporated with DENV luciferase reporter replicon RNAs. 24 hours post-electroporation, media was replaced with 3MA supplemented with oleic acid conjugated to BSA or BSA alone. 24 hours after addition of the drug, cells were lysed and the amount of DENV replication was assayed via luciferase assay. (B & C) Huh-7.5 cells were infected for four hours (MOI=0.5), then virus was removed and 3MA was applied at the indicated concentrations. The media was supplemented with an oleic acid-BSA conjugate or BSA alone. 48 hours post infection, (B) total RNA or (C) infectious DENV production was quantified. (D & E) Huh-7.5 cells were treated with the indicated siRNAs, maintained for 24 hours, then mock- or DENV-infected (MOI=2) for 24 hours, then (D) DENV RNA or (E) infectious DENV was quantified. (F). Huh-7.5 cells were infected for four hours (MOI=0.5), then virus was removed and the indicated inhibitors were applied. 24 hours after addition of the drug, DENV RNA was quantified. *p≤0.05.