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Translation initiation in the hepatitis C virus ( HCV ) occurs through a cap‐independent mechanism that involves an internal ribosome entry site ( IRES ) capable of interacting with and utilizing the eukaryotic translational machinery. In this review, we focus on the structural configuration of the different  HCV IRES  domains and the impact of  IRES  primary sequence variations on secondary structure conservation and function. In some cases, multiple mutations, even those scattered across different domains, led to restoration of the translational activity of the  HCV IRES , although the individual occurrences of these mutations were found to be deleterious. We propose that such observation may be attributed to probable long‐range inter‐ and/or intra‐domain functional interactions. The precise functioning of the  HCV IRES  requires the specific interaction of its domains with ribosomal subunits and a subset of eukaryotic translation initiation factors ( eIFs ). The structural conformation, sequence preservation and variability, and translational machinery association with the  HCV IRES  regions are also thoroughly discussed, along with other factors that can affect and influence the formation of translation initiation complexes.  WIREs RNA  2015, 6:211–224. doi: 10.1002/wrna.1268  This article is categorized under:  RNA Structure and Dynamics > Influence of RNA Structure in Biological Systems  Translation > Translation Regulation  RNA in Disease and Development > RNA in Disease

wiley interdisciplinary reviews: rna

Understanding the potential of hepatitis C virus internal ribosome entry site domains to modulate translation initiation via their structure and function