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. 2018 Jul 24;46(18):9776–9792. doi: 10.1093/nar/gky662

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© The Author(s) 2018. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 9. — Wild-type HCV genomic RNA replication is promoted by 5′ UTR targeting siRNAs in Ago2 knockout Huh-7.5 cells. (A and B) Show the sequence and western blot data confirming the knockout of the Ago2 gene in two independent cell lines generated using CRISPR/Cas9 technology. Ago2 knockout Huh-7.5 cells line A4 were co-electroporated with wild-type or G33C HCV RNA and the indicated small RNAs and miR-122 antagonist (anti-122) or control antagonist (anti-124). (C) Time course transient replication assay of wild-type HCV RNA in Ago2 knockout Huh-7.5 cell lines. Time course transient replication assay of the impact of the siRNA on wild-type HCV RNA in wild-type Huh-7.5 cells (D) and Ago2 knockout Huh-7.5 cells (E). (F) Shows potent siRNA stimulation of transient replication of wild-type HCV RNA in Ago2 knockout Huh-7.5 cells when miR-122 activity is abolished by using a miR-122 antagonist and (G) shows potent stimulation of transient replication of G33C by si18-36 G33C in Ago2 knockout cells when miR-122 activity is abolished.