ArticlePLoS pathogens2006
Host-specific response to HCV infection in the chimeric SCID-beige/Alb-uPA mouse model: role of the innate antiviral immune response.
Article in PLoS pathogens, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 76 citations in OpenAlex.
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- HCV and flaviviruses hijack cellular mechanisms for nuclear STAT2 degradation: Up-regulation of PDLIM2 suppresses the innate immune response.PLoS pathogens · 2019Article
- Murine Models of Hepatitis A Virus Infection.Cold Spring Harbor perspectives in medicine · 2019Review
- Prion Protein PRNP: A New Player in Innate Immunity? The Aβ Connection.Journal of Alzheimer's disease reports · 2017Article
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- Oxidative Stress Attenuates Lipid Synthesis and Increases Mitochondrial Fatty Acid Oxidation in Hepatoma Cells Infected with Hepatitis C Virus.The Journal of biological chemistry · 2016Article
- Intrinsic Viral Factors Are the Dominant Determinants of the Hepatitis C Virus Response to Interferon Alpha Treatment in Chimeric Mice.PloS one · 2016Article
- Impact of lipids and lipoproteins on hepatitis C virus infection and virus neutralization.World journal of gastroenterology · 2014Review
- The bacterial pathogen Listeria monocytogenes and the interferon family: type I, type II and type III interferons.Frontiers in cellular and infection microbiology · 2014Review
- Hepatitis C virus-induced cytoplasmic organelles use the nuclear transport machinery to establish an environment conducive to virus replication.PLoS pathogens · 2013Article
- A proautophagic antiviral role for the cellular prion protein identified by infection with a herpes simplex virus 1 ICP34.5 mutant.Journal of virology · 2013Article
- IFITM1 is a tight junction protein that inhibits hepatitis C virus entry.Hepatology (Baltimore, Md.) · 2013Article
- Article
- Hepatitis C virus infection and related liver disease: the quest for the best animal model.Frontiers in microbiology · 2013Article
- Functional mechanisms of the cellular prion protein (PrP(C)) associated anti-HIV-1 properties.Cellular and molecular life sciences : CMLS · 2012Article
- Establishment of a novel permissive cell line for the propagation of hepatitis C virus by expression of microRNA miR122.Journal of virology · 2012Article
- Novel small-molecule inhibitors of hepatitis C virus entry block viral spread and promote viral clearance in cell culture.PloS one · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
The severe combined immunodeficiency disorder (SCID)-beige/albumin (Alb)-urokinase plasminogen activator (uPA) mouse containing a human-mouse chimeric liver is currently the only small animal model capable of supporting hepatitis C virus (HCV) infection. This model was utilized to characterize the host transcriptional response to HCV infection. The purpose of these studies was to investigate the genetic component of the host response to HCV infection and also to distinguish virus-induced gene expression changes from adaptive HCV-specific immune-mediated effects. Gene expression profiles from HCV-infected mice were also compared to those from HCV-infected patients. Analyses of the gene expression data demonstrate that host factors regulate the response to HCV infection, including the nature of the innate antiviral immune response. They also indicate that HCV mediates gene expression changes, including regulation of lipid metabolism genes, which have the potential to be directly cytopathic, indicating that liver pathology may not be exclusively mediated by HCV-specific adaptive immune responses. This effect appears to be inversely related to the activation of the innate antiviral immune response. In summary, the nature of the initial interferon response to HCV infection may determine the extent of viral-mediated effects on host gene expression.
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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.