ArticleNucleic acids research2015
Inhibition of HCV translation by disrupting the structure and interactions of the viral CRE and 3' X-tail.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed.
- Interdependent RNA structural motifs at the 3'-terminus of the West Nile virus genome regulate viral growth.Nucleic acids research · 2026Article
- Article
- A ribosome-bound pseudoknot in the HCV coding region stimulates viral growth by tuning viral translation.Cell reports · 2026Article
- Hepatitis C virus NS3 helicase contributes to (-) strand RNA synthesis.Nature communications · 2025Article
- Strategies and efforts in circumventing the emergence of antiviral resistance against conventional antivirals.npj antimicrobials and resistance · 2025Review
- The West Nile virus genome harbors essential riboregulatory elements with conserved and host-specific functional roles.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Positive strand RNA viruses differ in the constraints they place on the folding of their negative strand.RNA (New York, N.Y.) · 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
- Structured elements drive extensive circular RNA translation.Molecular cell · 2021Article
- Comprehensive in vivo secondary structure of the SARS-CoV-2 genome reveals novel regulatory motifs and mechanisms.Molecular cell · 2021Article
- 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
- Ribosome Pausing at Inefficient Codons at the End of the Replicase Coding Region Is Important for Hepatitis C Virus Genome Replication.International journal of molecular sciences · 2020Article
- Hepatitis C Virus Translation Regulation.International journal of molecular sciences · 2020Review
- The multifarious roles of heterogeneous ribonucleoprotein A1 in viral infections.Reviews in medical virology · 2020Review
- The Role of the RNA-RNA Interactome in the Hepatitis C Virus Life Cycle.International journal of molecular sciences · 2020Review
- Structure and function analysis of the essential 3'X domain of hepatitis C virus.RNA (New York, N.Y.) · 2020Article
- Structural and phenotypic analysis of Chikungunya virus RNA replication elements.Nucleic acids research · 2019Article
- The HCV genome domains 5BSL3.1 and 5BSL3.3 act as managers of translation.Scientific reports · 2018Article
- Form confers function: Case of the 3'X region of the hepatitis C virus genome.World journal of gastroenterology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
A phylogenetically conserved RNA structure within the NS5B coding region of hepatitis C virus functions as a cis-replicating element (CRE). Integrity of this CRE, designated SL9266 (alternatively 5BSL3.2), is critical for genome replication. SL9266 forms the core of an extended pseudoknot, designated SL9266/PK, involving long distance RNA-RNA interactions between unpaired loops of SL9266 and distal regions of the genome. Previous studies demonstrated that SL9266/PK is dynamic, with 'open' and 'closed' conformations predicted to have distinct functions during virus replication. Using a combination of site-directed mutagenesis and locked nucleic acids (LNA) complementary to defined domains of SL9266 and its interacting regions, we have explored the influence of this structure on genome translation and replication. We demonstrate that LNAs which block formation of the closed conformation inhibit genome translation. Inhibition was at least partly independent of the initiation mechanism, whether driven by homologous or heterologous internal ribosome entry sites or from a capped message. Provision of SL9266/PK in trans relieved translational inhibition, and mutational analysis implied a mechanism in which the closed conformation recruits a cellular factor that would otherwise suppresses translation. We propose that SL9266/PK functions as a temporal switch, modulating the mutually incompatible processes of translation and replication.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.