ArticleJournal of virology2008
Vectorial entry and release of hepatitis A virus in polarized human hepatocytes.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 48 citations in OpenAlex.
- The hepatocyte traffic network in the human hepatitis A virus biological cycle from an evolutionary perspective.Communications biology · 2025Article
- Liver Organoid Potential Application for Hepatitis E Virus Infection.Advances in experimental medicine and biology · 2023Article
- Review
- Viral Hepatitis - The Road Traveled and the Journey Remaining.Hepatic medicine : evidence and research · 2022Review
- Egress of non-enveloped enteric RNA viruses.The Journal of general virology · 2021Review
- Review
- Cell Culture Models for Hepatitis E Virus.Viruses · 2019Review
- Stem Cell-Derived Culture Models of Hepatitis E Virus Infection.Cold Spring Harbor perspectives in medicine · 2019Review
- Vectorial Release of Hepatitis E Virus in Polarized Human Hepatocytes.Journal of virology · 2019Article
- Hepatitis A Virus Genome Organization and Replication Strategy.Cold Spring Harbor perspectives in medicine · 2018Review
- Entry and Release of Hepatitis C Virus in Polarized Human Hepatocytes.Journal of virology · 2017Article
- PI3K/SHIP2/PTEN pathway in cell polarity and hepatitis C virus pathogenesis.World journal of hepatology · 2017Review
- Article
- Specific IgA Enhances the Transcytosis and Excretion of Hepatitis A Virus.Scientific reports · 2016Article
- New Methods in Tissue Engineering: Improved Models for Viral Infection.Annual review of virology · 2014Article
- Molecular biology and inhibitors of hepatitis A virus.Medicinal research reviews · 2014Review
- SHIP2 regulates epithelial cell polarity through its lipid product, which binds to Dlg1, a pathway subverted by hepatitis C virus core protein.Molecular biology of the cell · 2013Article
- Hepatitis C virus replication and Golgi function in brefeldin a-resistant hepatoma-derived cells.PloS one · 2013Article
- Hepatocyte polarity.Comprehensive Physiology · 2013Review
- Hepatocytes traffic and export hepatitis B virus basolaterally by polarity-dependent mechanisms.Journal of virology · 2011Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis A virus (HAV) is an enterically transmitted virus that replicates predominantly in hepatocytes within the liver before excretion via bile through feces. Hepatocytes are polarized epithelial cells, and it has been assumed that the virus load in bile results from direct export of HAV via the apical domain of polarized hepatocytes. We have developed a subclone of hepatocyte-derived HepG2 cells (clone N6) that maintains functional characteristics of polarized hepatocytes but displays morphology typical of columnar epithelial cells, rather than the complex morphology that is typical of hepatocytes. N6 cells form microcolonies of polarized cells when grown on glass and confluent monolayers of polarized cells on semipermeable membranes. When N6 microcolonies were exposed to HAV, infection was restricted to peripheral cells of polarized colonies, whereas all cells could be infected in colonies of nonpolarized HepG2 cells (clone C11) or following disruption of tight junctions in N6 colonies with EGTA. This suggests that viral entry occurs predominantly via the basolateral plasma membrane, consistent with uptake of virus from the bloodstream after enteric exposure, as expected. Viral export was also found to be markedly vectorial in N6 but not C11 cells. However, rather than being exported from the apical domain as expected, more than 95% of HAV was exported via the basolateral domain of N6 cells, suggesting that virus is first excreted from infected hepatocytes into the bloodstream rather than to the biliary tree. Enteric excretion of HAV may therefore rely on reuptake and transcytosis of progeny HAV across hepatocytes into the bile. These studies provide the first example of the interactions between viruses and polarized hepatocytes.
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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.