ArticleThe American journal of pathology2003
Dynamics of hepatitis C virus replication in human liver.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 63 citations in OpenAlex.
- Quantifying the diversification of hepatitis C virus (HCV) during primary infection: estimates of the in vivo mutation rate.PLoS pathogens · 2012Trial
- Burden, Outcome, and Comorbidities of Extrahepatic Manifestations in Hepatitis C Virus Infection.Biology · 2022Review
- Review
- HCV reflex testing: A single-sample, low-contamination method that improves the diagnostic efficiency of HCV testing among patients in Alberta, Canada.Journal of the Association of Medical Microbiology and Infectious Disease Canada = Journal officiel de l'Association pour la microbiologie medicale et l'infectiologie Canada · 2022Article
- Evidence for Internal Initiation of RNA Synthesis by the Hepatitis C Virus RNA-Dependent RNA Polymerase NS5BJournal of virology · 2019Article
- Repeated spontaneous clearance of hepatitis C virus infection in the setting of long-term non-progression of HIV infection.Infectious disease reports · 2017Article
- Oligonucleotide-Lipid Conjugates Forming G-Quadruplex Structures Are Potent and Pangenotypic Hepatitis C Virus Entry InhibitorsAntimicrobial agents and chemotherapy · 2017Article
- Modeling Viral Spread.Annual review of virology · 2016Review
- Long noncoding RNA EGOT negatively affects the antiviral response and favors HCV replication.EMBO reports · 2016Article
- Lipoprotein Receptors Redundantly Participate in Entry of Hepatitis C Virus.PLoS pathogens · 2016Article
- Identification of a Potent and Broad-Spectrum Hepatitis C Virus Fusion Inhibitory Peptide from the E2 Stem Domain.Scientific reports · 2016Article
- New Insights into the Understanding of Hepatitis C Virus Entry and Cell-to-Cell Transmission by Using the Ionophore Monensin A.Journal of virology · 2015Article
- Spatiotemporal analysis of hepatitis C virus infection.PLoS pathogens · 2015Article
- Inferring viral dynamics in chronically HCV infected patients from the spatial distribution of infected hepatocytes.PLoS computational biology · 2014Article
- CD81 and hepatitis C virus (HCV) infection.Viruses · 2014Review
- Next-generation sequencing reveals large connected networks of intra-host HCV variants.BMC genomics · 2014Article
- Cell-cell contact-mediated hepatitis C virus (HCV) transfer, productive infection, and replication and their requirement for HCV receptors.Journal of virology · 2013Article
- Inhibition of hepatitis C virus (HCV) replication by specific RNA aptamers against HCV NS5B RNA replicase.Journal of virology · 2013Article
- Preclinical evaluation of an anti-HCV miRNA cluster for treatment of HCV infection.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Analysis of the virus dynamics model reveals that early treatment of HCV infection may lead to the sustained virological response.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
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Hepatitis C virus (HCV) replication at the cellular level is not fully understood. This study describes an optimized system for quantifying replication of HCV in hepatocytes and in liver tissues. A digital image analysis method was developed to quantify signal intensities of HCV genomic and replicative-intermediate RNAs in infected human liver tissues and to examine their spatial distribution. The average number of viral genomes per productively infected hepatocyte ranged from 7 to 64 RNA molecules. The maximal concentrations of genomic and replicative-intermediate RNAs at the single cell level were 74 and 34 molecules per hepatocyte, respectively. A gradient dispersion of genomes was observed around virus-producing cells, suggesting infection of neighboring hepatocytes as one mechanism of viral spread in the liver. There was no significant difference in total hepatic load of HCV genomes between the post- and nontransplant patients, whereas serum titers in the former group were much higher that that in the latter group. HCV replication varied among infected hepatocytes, occurred in a subset of cells, and proceeded at a low level, confirming one mechanism by which individual hepatocytes are cumulatively able to generate steady state concentrations of millions of HCV genomes per milliliter of blood. Lower viral clearance rates in circulating blood may explain the phenomenon of increased serum titers of viral RNA in posttransplant immunosuppressed patients.
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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.