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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: Virology. 2017 Apr 26;507:231–241. doi: 10.1016/j.virol.2017.04.014

Fig. 8. A model for the interaction of DDX6 and miR-122 with the HCV genome.

Fig. 8

Early during HCV infection the positive-sense RNA genome acts as transcript for translation of viral proteins, and later is used as a template for replication of the viral genome. (A–B) The transition from translation to replication is closely regulated by components within viral RNA secondary structure, displacement of PCBP2, and binding of host miR-122, and host and viral proteins. (C) In this study we also show that depletion of DDX6 affects the interaction of miR-122 with site 2 in the 5′ UTR to decrease HCV RNA stability, and that by modulating the interaction of miR-122 with the 5′ UTR, DDX6 is a key regulator in the switch between translation and replication, where depletion of DDX6 delays the transition to and initiation of replication.