ArticleProceedings of the National Academy of Sciences of the United States of America2007
Cellular cofactors affecting hepatitis C virus infection and replication.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 296 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
296 citing papers in PubMed, 526 citations in OpenAlex.
- Acute Hepatitis C Virus Infection Induces Consistent Changes in Circulating MicroRNAs That Are Associated with Nonlytic Hepatocyte Release.Journal of virology · 2015Trial
- In vitro antiviral activity and preclinical and clinical resistance profile of miravirsen, a novel anti-hepatitis C virus therapeutic targeting the human factor miR-122.Antimicrobial agents and chemotherapy · 2015Trial
- Genome-wide RNAi screen reveals a new role of a WNT/CTNNB1 signaling pathway as negative regulator of virus-induced innate immune responses.PLoS pathogens · 2013Trial
- Shared host genetic landscape of respiratory viral infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Development and characterization of a miRNA-responsive circular RNA expression system with cell type specificity.Molecular therapy. Nucleic acids · 2025Article
- MicroRNA biogenesis is broadly disrupted by inhibition of the splicing factor SF3B1.Nucleic acids research · 2024Article
- Article
- Roles of epidermal growth factor receptor, claudin-1 and occludin in multi-step entry of hepatitis C virus into polarized hepatoma spheroids.PLoS pathogens · 2023Article
- Several cell-intrinsic effectors drive type I interferon-mediated restriction of HIV-1 in primary CD4Cell reports · 2023Article
- Therapeutic interventions of acute and chronic liver disorders: A comprehensive review.World journal of hepatology · 2023Review
- MicroRNAs: Small Molecules with Significant Functions, Particularly in the Context of Viral Hepatitis B and C Infection.Medicina (Kaunas, Lithuania) · 2023Review
- Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.Journal of medicinal chemistry · 2022Article
- Article
- MicroRNA-122 Regulation of HCV Infections: Insights from Studies of miR-122-Independent Replication.Pathogens (Basel, Switzerland) · 2022Review
- Investigating the Human Host-ssRNA Virus Interaction Landscape Using the SMEAGOL Toolbox.Viruses · 2022Article
- Functional Assessment of Stroke-Induced Regulation of miR-20a-3p and Its Role as a Neuroprotectant.Translational stroke research · 2022Article
- Article
- The multifaceted roles of NLRP3-modulating proteins in virus infection.Frontiers in immunology · 2022Review
- A Novel Small Molecule Inhibits Hepatitis C Virus Propagation in Cell Culture.Microbiology spectrum · 2021Article
- Article
236 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
20 authors at 8 institutions in 2 countries.
Funding
Abstract
Recently identified hepatitis C virus (HCV) isolates that are infectious in cell culture provide a genetic system to evaluate the significance of virus-host interactions for HCV replication. We have completed a systematic RNAi screen wherein siRNAs were designed that target 62 host genes encoding proteins that physically interact with HCV RNA or proteins or belong to cellular pathways thought to modulate HCV infection. This includes 10 host proteins that we identify in this study to bind HCV NS5A. siRNAs that target 26 of these host genes alter infectious HCV production >3-fold. Included in this set of 26 were siRNAs that target Dicer, a principal component of the RNAi silencing pathway. Contrary to the hypothesis that RNAi is an antiviral pathway in mammals, as has been reported for subgenomic HCV replicons, siRNAs that target Dicer inhibited HCV replication. Furthermore, siRNAs that target several other components of the RNAi pathway also inhibit HCV replication. MicroRNA profiling of human liver, human hepatoma Huh-7.5 cells, and Huh-7.5 cells that harbor replicating HCV demonstrated that miR-122 is the predominant microRNA in each environment. miR-122 has been previously implicated in positively regulating the replication of HCV genotype 1 replicons. We find that 2'-O-methyl antisense oligonucleotide depletion of miR-122 also inhibits HCV genotype 2a replication and infectious virus production. Our data define 26 host genes that modulate HCV infection and indicate that the requirement for functional RNAi for HCV replication is dominant over any antiviral activity this pathway may exert against HCV.
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.