ArticleRNA (New York, N.Y.)2009
A long-range RNA-RNA interaction between the 5' and 3' ends of the HCV genome.
Article in RNA (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 124 citations in OpenAlex.
- Decoding the Structural Complexity of Viral RNAs with SHAPE to Guide Antiviral Therapeutics.Viruses · 2026Review
- Hepatitis C Virus 5'UTR Sequences That Bind eIF3 and Ribosomal 40S Subunits Confer Stimulation of Minus-Strand RNA Synthesis.International journal of molecular sciences · 2026Article
- A ribosome-bound pseudoknot in the HCV coding region stimulates viral growth by tuning viral translation.Cell reports · 2026Article
- The mutational landscape of SARS-CoV-2 provides new insight into viral evolution and fitness.Nature communications · 2025Article
- Conformational dynamics of the hepatitis C virus 3'X RNA.RNA (New York, N.Y.) · 2024Article
- The 3' end of the coding region of senecavirus A contains a highly conserved sequence that potentially forms a stem-loop structure required for virus rescue.Archives of virology · 2023Article
- Dimerization of an umbravirus RNA genome activates subgenomic mRNA transcription.Nucleic acids research · 2023Article
- RNA levers and switches controlling viral gene expression.Trends in biochemical sciences · 2023Review
- Inter- and Intramolecular RNA-RNA Interactions Modulate the Regulation of Translation Mediated by the 3' UTR in West Nile Virus.International journal of molecular sciences · 2023Article
- The Genomic 3' UTR of Flaviviruses Is a Translation Initiation Enhancer.International journal of molecular sciences · 2022Article
- Identification and characterization of virus-encoded circular RNAs in host cells.Microbial genomics · 2022Article
- TheJournal of virology · 2022Article
- The low-resolution structural models of hepatitis C virus RNA subdomain 5BSL3.2 and its distal complex with domain 3'X point to conserved regulatory mechanisms within the Flaviviridae family.Nucleic acids research · 2022Article
- The tale of two flaviviruses: subversion of host pathways by RNA shapes in dengue and hepatitis C viral RNA genomes.Current opinion in microbiology · 2021Review
- Activation of viral transcription by stepwise largescale folding of an RNA virus genome.Nucleic acids research · 2020Article
- Hepatitis C Virus Translation Regulation.International journal of molecular sciences · 2020Review
- Hepatitis C Virus Replication.Cold Spring Harbor perspectives in medicine · 2020Review
- The Role of the RNA-RNA Interactome in the Hepatitis C Virus Life Cycle.International journal of molecular sciences · 2020Review
- Article
- Interaction of coronavirus nucleocapsid protein with the 5'- and 3'-ends of the coronavirus genome is involved in genome circularization and negative-strand RNA synthesis.The FEBS journal · 2019Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RNA genome of the hepatitis C virus (HCV) contains multiple conserved structural cis domains that direct protein synthesis, replication, and infectivity. The untranslatable regions (UTRs) play essential roles in the HCV cycle. Uncapped viral RNAs are translated via an internal ribosome entry site (IRES) located at the 5' UTR, which acts as a scaffold for recruiting multiple protein factors. Replication of the viral genome is initiated at the 3' UTR. Bioinformatics methods have identified other structural RNA elements thought to be involved in the HCV cycle. The 5BSL3.2 motif, which is embedded in a cruciform structure at the 3' end of the NS5B coding sequence, contributes to the three-dimensional folding of the entire 3' end of the genome. It is essential in the initiation of replication. This paper reports the identification of a novel, strand-specific, long-range RNA-RNA interaction between the 5' and 3' ends of the genome, which involves 5BSL3.2 and IRES motifs. Mutants harboring substitutions in the apical loop of domain IIId or in the internal loop of 5BSL3.2 disrupt the complex, indicating these regions are essential in initiating the kissing interaction. No complex was formed when the UTRs of the related foot and mouth disease virus were used in binding assays, suggesting this interaction is specific for HCV sequences. The present data firmly suggest the existence of a higher-order structure that may mediate a protein-independent circularization of the HCV genome. The 5'-3' end bridge may have a role in viral translation modulation and in the switch from protein synthesis to RNA replication.
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