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. Author manuscript; available in PMC: 2015 Feb 1.
Published in final edited form as: Nat Med. 2014 Jul 27;20(8):927–935. doi: 10.1038/nm.3610

Figure 3.

Figure 3

Inhibition of lipid peroxidation by SKI or VE promotes production and spread of infectious genotype 1 HCV. (a) Infectious virus yields from Huh-7.5 cells transfected with the indicated viral RNAs and grown in the presence of 1 μM SKI, 1 μM VE or DMSO vehicle. Culture supernatant fluids were harvested and replaced with fresh media containing compounds every 24 h. Infectivity titers are expressed as focus forming units (FFU) ml−1. Data shown are mean ± s.e.m. from three replicate cultures. (b) SKI promotes spread of H77S.3 but inhibits HJ3-5 virus. Cells electroporated with H77S.3 or HJ3-5 RNAs were mixed with carboxyfluorescein succinimidyl ester (CFSE)-labeled naïve Huh-7.5 cells; CFSE/NS5A double-positive cells (upper right quadrant) are indicative of virus spread. (c) Buoyant density of H77S.3 virus particles released from H77S.3 RNA-transfected Huh-7.5 cells grown in 1 μM SKI (left) or 1 μM VE (right) vs. DMSO control. Fractions from isopycnic iodixanol gradients were assayed for infectious virus (FFU) or HCV RNA (GE = genome equivalents). The data shown are representative of two independent experiments.