ArticleJournal of virology2006
Replication of hepatitis C virus (HCV) RNA in mouse embryonic fibroblasts: protein kinase R (PKR)-dependent and PKR-independent mechanisms for controlling HCV RNA replication and mediating interferon activities.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 92 citations in OpenAlex.
- Receptor transporter protein 4 (RTP4)-mediated repression of hepatitis C virus replication in mouse cells.PLoS pathogens · 2025Article
- Animal Models of Hepatitis C Virus Infection.Cold Spring Harbor perspectives in medicine · 2020Review
- Differences across cyclophilin A orthologs contribute to the host range restriction of hepatitis C virus.eLife · 2019Article
- Hepatitis C virus cell culture models: an encomium on basic research paving the road to therapy development.Medical microbiology and immunology · 2019Review
- Attachment and Postattachment Receptors Important for Hepatitis C Virus Infection and Cell-to-Cell Transmission.Journal of virology · 2017Article
- Article
- HCV derived from sera of HCV-infected patients induces pro-fibrotic effects in human primary fibroblasts by activating GLI2.Scientific reports · 2016Article
- Viral genome imaging of hepatitis C virus to probe heterogeneous viral infection and responses to antiviral therapies.Virology · 2016Article
- Viral hepatitis: HCV compartmentalization in HCC: driver, passenger or both?Nature reviews. Gastroenterology & hepatology · 2016Article
- The Serum Very-Low-Density Lipoprotein Serves as a Restriction Factor against Hepatitis C Virus Infection.Journal of virology · 2015Article
- Hepatitis C virus and antiviral innate immunity: who wins at tug-of-war?World journal of gastroenterology · 2015Review
- 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
- Infection of Human Liver Myofibroblasts by Hepatitis C Virus: A Direct Mechanism of Liver Fibrosis in Hepatitis C.PloS one · 2015Article
- Persistent hepatitis C virus infections and hepatopathological manifestations in immune-competent humanized mice.Cell research · 2014Article
- Visualizing hepatitis C virus infection in humanized mice.Journal of immunological methods · 2014Review
- Specific sequence of a Beta turn in human la protein may contribute to species specificity of hepatitis C virus.Journal of virology · 2014Article
- Murine models of hepatitis C: what can we look forward to?Antiviral research · 2014Review
- Protein kinase expression as a predictive factor for interferon response in chronic hepatitis C patients.Journal of advanced research · 2014Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Hepatitis C virus (HCV) infection causes chronic hepatitis and is currently treated with alpha interferon (IFN-alpha)-based therapies. The underlying mechanisms of chronic HCV infection and IFN-based therapies, however, have not been defined. Protein kinase R (PKR) was implicated in the control of HCV replication and mediation of IFN-induced antiviral response. In this report, we demonstrate that a subgenomic RNA replicon of genotype 2a HCV replicated efficiently in mouse embryonic fibroblasts (MEFs), as determined by cell colony formation efficiency and the detection of HCV proteins and both positive- and negative-strand RNAs. Additionally, the subgenomic HCV RNA was found to replicate more efficiently in the PKR knockout (PKR(-/-)) MEF than in the wild-type (PKR(+/+)) MEF. The knockdown expression of PKR by specific small interfering RNAs significantly enhanced the level of HCV RNA replication, suggesting that PKR is involved in the control of HCV RNA replication. The level of ISG56 (p56) was induced by HCV RNA replication, indicating the activation of PKR-independent antiviral pathways. Furthermore, IFN-alpha/beta inhibited HCV RNA replication in PKR(-/-) MEFs as efficiently as in PKR(+/+) MEFs. These findings demonstrate that PKR-independent antiviral pathways play important roles in controlling HCV replication and mediating IFN-induced antiviral effect. Our findings also provide a foundation for the development of transgenic mouse models of HCV replication and set a stage to further define the roles of cellular genes in the establishment of chronic HCV infection and the mediation of intracellular innate antiviral response by using MEFs derived from diverse gene knockout animals.
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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.