ArticlePloS one2009
Focal distribution of hepatitis C virus RNA in infected livers.
Article in PloS one, 2009. 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.
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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, 58 citations in OpenAlex.
- Assessment of hepatitis C virus permissiveness in iteratively genetically humanized mice.Journal of virology · 2025Article
- Hepatocytes and the art of killing Plasmodium softly.Trends in parasitology · 2024Review
- MicroRNA-122 Regulation of HCV Infections: Insights from Studies of miR-122-Independent Replication.Pathogens (Basel, Switzerland) · 2022Review
- MicroRNA 122 Affects both the Initiation and the Maintenance of Hepatitis C Virus Infections.Journal of virology · 2022Article
- HCV Spread Kinetics Reveal Varying Contributions of Transmission Modes to Infection Dynamics.Viruses · 2021Article
- HIV influences clustering and intracellular replication of hepatitis C virus.Journal of viral hepatitis · 2021Article
- Complex patterns of Hepatitis-C virus longitudinal clustering in a high-risk population.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2018Article
- Article
- Transcriptional response to hepatitis C virus infection and interferon-alpha treatment in the human liver.EMBO molecular medicine · 2017Article
- Review
- High resolution sequencing of hepatitis C virus reveals limited intra-hepatic compartmentalization in end-stage liver disease.Journal of hepatology · 2017Article
- Modeling Viral Spread.Annual review of virology · 2016Review
- Exceptional Heterogeneity in Viral Evolutionary Dynamics Characterises Chronic Hepatitis C Virus Infection.PLoS pathogens · 2016Article
- Long noncoding RNA EGOT negatively affects the antiviral response and favors HCV replication.EMBO reports · 2016Article
- Diminished viral replication and compartmentalization of hepatitis C virus in hepatocellular carcinoma tissue.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Inferring viral dynamics in chronically HCV infected patients from the spatial distribution of infected hepatocytes.PLoS computational biology · 2014Article
- Visualizing hepatitis C virus infection in humanized mice.Journal of immunological methods · 2014Review
- Simultaneous detection of hepatitis C virus and interferon stimulated gene expression in infected human liver.Hepatology (Baltimore, Md.) · 2014Article
- Unfolded protein response in hepatitis C virus infection.Frontiers in microbiology · 2014Review
- Single cell analysis of HCV-infected patient hepatocytes: the science is no longer science fiction.Gastroenterology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatitis C virus (HCV) is a plus-strand RNA virus that replicates by amplification of genomic RNA from minus strands leading to accumulation of almost one thousand copies per cell under in vitro cell culture conditions. In contrast, HCV RNA copy numbers in livers of infected patients appear to be much lower, estimated at a few copies per cell. METHODOLOGY/PRINCIPAL
findingsTo gain insights into mechanisms that control HCV replication in vivo, we analyzed HCV RNA levels as well as expression of interferon beta (IFNbeta) and several interferon stimulated genes (ISGs) from whole liver sections and micro-dissected subpopulations of hepatocytes in biopsy samples from 21 HCV-infected patients. The results showed that intrahepatic HCV RNA levels range form less than one copy per hepatocyte to a maximum of about eight. A correlation existed between viral RNA levels and IFNbeta expression, but not between viral RNA and ISG levels. Also, IFNbeta expression did not correlate with ISGs levels. Replication of HCV RNA occurred in focal areas in the liver in the presence of a general induction of ISGs. CONCLUSION/SIGNIFICANCE: The low average levels of HCV RNA in biopsy samples can be explained by focal distribution of infected hepatocytes. HCV replication directly induces IFNbeta, which then activates ISGs. The apparent lack of a correlation between levels of IFNbeta and ISG expression indicates that control of the innate immune response during HCV infections depends on multiple factors.
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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.