ArticleJournal of virology2011
ISG56 and IFITM1 proteins inhibit hepatitis C virus replication.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
What it found
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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.
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Who cites it
96 citing papers in PubMed, 150 citations in OpenAlex.
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- MicroRNA-122 protects against interferon-α-induced hepatic inflammatory response via the Janus kinase-signal transducer and activator of transcription pathway.Endocrine journal · 2025Article
- Suppression of Innate Immunity by the Hepatitis C Virus (HCV): Revisiting the Specificity of Host-Virus Interactive Pathways.International journal of molecular sciences · 2023Review
- The novel role of IFITM1-3 in myogenic differentiation of C2C12 cells.Intractable & rare diseases research · 2023Article
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- IFITM1 enhances nonenveloped viral RNA replication by facilitating cholesterol transport to the Golgi.PLoS pathogens · 2023Article
- DDX60 selectively reduces translation off viral type II internal ribosome entry sites.EMBO reports · 2022Article
- Toll-like receptor 3 signaling induces interferon-induced transmembrane protein 1 in BEAS-2B cells.Experimental biology and medicine (Maywood, N.J.) · 2022Article
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- A Human and Rhesus Macaque Interferon-Stimulated Gene Screen Shows That Over-Expression ofViruses · 2022Article
- Lessons in self-defence: inhibition of virus entry by intrinsic immunity.Nature reviews. Immunology · 2022Review
- Article
- Interferon Control of Human Coronavirus Infection and Viral Evasion: Mechanistic Insights and Implications for Antiviral Drug and Vaccine Development.Journal of molecular biology · 2022Review
- The Role of IFITM Proteins in Tick-Borne Encephalitis Virus Infection.Journal of virology · 2022Article
- Article
- IKKε isoform switching governs the immune response against EV71 infection.Communications biology · 2021Article
- Melatonin Inhibits Dengue Virus Infection via the Sirtuin 1-Mediated Interferon Pathway.Viruses · 2021Article
- Review
- Crosstalk Between SUMO and Ubiquitin-Like Proteins: Implication for Antiviral Defense.Frontiers in cell and developmental biology · 2021Review
36 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
Hepatitis C virus (HCV) often leads to persistent infection. Interferon (IFN) and IFN-stimulated genes (ISGs) are amplified during HCV infection but fail to eliminate virus from the liver in a large number of infected patients. We have observed previously that HCV infection induces IFN-β production in immortalized human hepatocytes (IHH) as early as 24 h after infection, although virus replication is not inhibited. To gain insights on possible countermeasures of virus for the suppression of host antiviral response, the cellular transcriptional profiles of ISGs were examined after various treatments of IHH. The majority of ISGs were upregulated in IFN-treated IHH from the level for mock-treated cells. However, the comparison of ISG expression in IFN-treated IHH and IFN-pretreated, HCV genotype 2a-infected IHH indicated that virus infection suppresses the upregulation of a subset of effector molecules, including ISG56 and IFITM1. Similar results were observed for HCV-infected Huh7 cells. Subsequent study suggested that the exogenous expression of ISG56 or IFITM1 inhibits HCV replication in IHH or Huh7 cells, and the knockdown of these genes enhanced HCV replication. Further characterization revealed that the overexpression of these ISGs does not block HCV pseudotype entry into Huh7 cells. Taken together, our results demonstrated that ISG56 and IFITM1 serve as important molecules to restrict HCV infection, and they may have implications in the development of therapeutic modalities.
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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.