ArticleJournal of virology2010
Replication of subgenomic hepatitis C virus replicons in mouse fibroblasts is facilitated by deletion of interferon regulatory factor 3 and expression of liver-specific microRNA 122.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 63 citations in OpenAlex.
- Receptor transporter protein 4 (RTP4)-mediated repression of hepatitis C virus replication in mouse cells.PLoS pathogens · 2025Article
- The involvement of microRNAs in HCV and HIV infection.Therapeutic advances in vaccines and immunotherapy · 2022Review
- The Methanolic Extract ofViruses · 2021Article
- Animal Models of Hepatitis C Virus Infection.Cold Spring Harbor perspectives in medicine · 2020Review
- Establishment and Characterization of a New Cell Line Permissive for Hepatitis C Virus Infection.Scientific reports · 2019Article
- Differences across cyclophilin A orthologs contribute to the host range restriction of hepatitis C virus.eLife · 2019Article
- A preliminary analysis of hepatitis C virus in pancreatic islet cells.Virology journal · 2017Article
- Article
- (4R,6S)-2-Dihydromenisdaurilide is a Butenolide that Efficiently Inhibits Hepatitis C Virus Entry.Scientific reports · 2016Article
- Cell culture-derived HCV cannot infect synovial fibroblasts.Scientific reports · 2015Article
- Control of hepatitis C virus replication in mouse liver-derived cells by MAVS-dependent production of type I and type III interferons.Journal of virology · 2015Article
- Quantitative Proteomics Analysis of the Hepatitis C Virus Replicon High-Permissive and Low-Permissive Cell Lines.PloS one · 2015Article
- Mechanisms of HCV-induced liver cancer: what did we learn from in vitro and animal studies?Cancer letters · 2014Review
- Murine models of hepatitis C: what can we look forward to?Antiviral research · 2014Review
- Specific sequence of a Beta turn in human la protein may contribute to species specificity of hepatitis C virus.Journal of virology · 2014Article
- Apolipoprotein E codetermines tissue tropism of hepatitis C virus and is crucial for viral cell-to-cell transmission by contributing to a postenvelopment step of assembly.Journal of virology · 2014Article
- Interferon lambda: opportunities, risks, and uncertainties in the fight against HCV.Frontiers in immunology · 2014Review
- Transient replication of Hepatitis C Virus sub-genomic RNA in murine cell lines is enabled by miR-122 and varies with cell passage.PloS one · 2014Article
- Hepatitis C: a mouse at the end of the tunnel.Cell research · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Hepatitis C virus (HCV) infection causes significant morbidity, and efficient mouse models would greatly facilitate virus studies and the development of effective vaccines and new therapeutic agents. Entry factors, innate immunity, and host factors needed for viral replication represent the initial barriers that restrict HCV infection of mouse cells. Experiments in this paper consider early postentry steps of viral infection and investigate the roles of interferon regulatory factors (IRF-3 and IRF-9) and microRNA (miR-122) in promoting HCV replication in mouse embryo fibroblasts (MEFs) that contain viral subgenomic replicons. While wild-type murine fibroblasts are restricted for HCV RNA replication, deletion of IRF-3 alone can facilitate replicon activity in these cells. This effect is thought to be related to the inactivation of the type I interferon synthesis mediated by IRF-3. Additional deletion of IRF-9 to yield IRF-3(-/-) IRF-9(-/-) MEFs, which have blocked type I interferon signaling, did not increase HCV replication. Expression of liver-specific miR-122 in MEFs further stimulated the synthesis of HCV replicons in the rodent fibroblasts. The combined effects of miR-122 expression and deletion of IRF-3 produced a cooperative stimulation of HCV subgenome replication. miR-122 and IRF-3 are independent host factors that are capable of influencing HCV replication, and our findings could help to establish mouse models and other cell systems that support HCV growth and particle formation.
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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.