This basic science study demonstrates that functional IRES elements are crucial for BovHepV translation and that the host factor miR-122 enhances this process.
May guide antiviral strategies targeting IRES-miR-122 in hepaciviruses; leaves open translation from bovine models to human disease.
Several members of the family Flaviviridae , including HCV, have adapted cap-independent translation strategies to overcome canonical eukaryotic translation pathways and use cis -acting RNA-elements, designated viral internal ribosome entry sites (IRES), to initiate translation. Although novel hepaciviruses have been identified in different animal species, only limited information is available on their biology on molecular level. Therefore, our aim was a fundamental analysis of BovHepV IRES functions. The findings which show that functional IRES elements are also crucial for BovHepV translation expand our knowledge on molecular mechanism of hepacivirus propagation. We also studied the possible effects of one major host factor implicated in HCV pathogenesis, miR-122. The results of mutational analyses suggested that miR-122 enhances virus translation mediated by BovHepV IRES.
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Baron et al. (2018) studied Bovine Hepacivirus (BovHepV) translation. Mutational analysis and miR-122 was evaluated on BovHepV translation mediated by IRES.
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