Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 21, Issue 16, Pages -Publisher
MDPI
DOI: 10.3390/ijms21165677
Keywords
hepatitis C virus 1; microRNA 2; miR-122 3; replication 4; translation 5; RNA stabilization 6; tropism 7; pathogenesis 8
Funding
- Canadian Institutes of Health Research [MOP-133458]
- University of Saskatchewan College of Medicine Bridge Funding (CoMBRIDGE)
- Natural Sciences and Engineering Research Council of Canada [RGPIN-2018-06335]
- Canadian Network on Hepatitis C (CanHepC) Training Program, Doctoral Research Fellowships
- Natural Sciences and Engineering Research council of Canada, Undergraduate Summer Research Awards (NSERC-USRA)
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Hepatitis C virus (HCV) replication requires annealing of a liver specific microRNA, miR-122 to 2 sites on 5 ' untranslated region (UTR). While, microRNAs downregulate gene expression by binding to the 3 ' untranslated region of the target mRNA, in this case, the microRNA anneals to the 5 ' UTR of the viral genomes and upregulates the viral lifecycle. In this review, we explore the current understandings of the mechanisms by which miR-122 promotes the HCV lifecycle, and its contributions to pathogenesis. Annealing of miR-122 has been reported to (a) stimulate virus translation by promoting the formation of translationally active internal ribosome entry site (IRES) RNA structure, (b) stabilize the genome, and (c) induce viral genomic RNA replication. MiR-122 modulates lipid metabolism and suppresses tumor formation, and sequestration by HCV may influence virus pathogenesis. We also discuss the possible use of miR-122 as a biomarker for chronic hepatitis and as a therapeutic target. Finally, we discuss roles for miR-122 and other microRNAs in promoting other viruses.
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