ReviewBiochimica et biophysica acta. Biomembranes2020
Hepatitis C virus infection and tight junction proteins: The ties that bind.
Review in Biochimica et biophysica acta. Biomembranes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Exploring the Inhibitory Effects of Compounds for the Treatment of Liver Fibrosis: A Computational and Microscopic Approach.Current pharmaceutical design · 2026Article
- Review
- Newcastle disease virus promotes spreading infection through vimentin-dependent tight junction injury mediated by MLC/p-MLC activation.PLoS pathogens · 2025Article
- Claudin-11 plays a pivotal role in the clathrin-mediated endocytosis of influenza A virus.Science China. Life sciences · 2025Article
- HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus.Frontiers in immunology · 2025Review
- Exploring the role of YBX3 in PEDV infection through the utilization of YBX3 knockout and overexpression cell lines.Virus genes · 2024Article
- MiR-181a Negatively Regulates Claudin-3 to FacilitateViruses · 2024Article
- Contemporary Insights into Hepatitis C Virus: A Comprehensive Review.Microorganisms · 2024Review
- The Basic Requirement of Tight Junction Proteins in Blood-Brain Barrier Function and Their Role in Pathologies.International journal of molecular sciences · 2024Review
- Micronutrients at Supplemental Levels, Tight Junctions and Epithelial Barrier Function: A Narrative Review.International journal of molecular sciences · 2024Review
- USP40 promotes hepatocellular carcinoma cell proliferation, migration and stemness by deubiquitinating and stabilizing Claudin1.Biology direct · 2024Article
- Occludin: a gatekeeper of brain Infection by HIV-1.Fluids and barriers of the CNS · 2023Review
- Transcriptional Analysis of lncRNA and Target Genes Induced by Influenza A Virus Infection in MDCK Cells.Vaccines · 2023Article
- Improvement of wound healing by capsaicin through suppression of the inflammatory response and amelioration of the repair process.Molecular medicine reports · 2023Article
- Transcriptional and Epigenetic Alterations in the Progression of Non-Alcoholic Fatty Liver Disease and Biomarkers Helping to Diagnose Non-Alcoholic Steatohepatitis.Biomedicines · 2023Article
- Tight Junctions, the Key Factor in Virus-Related Disease.Pathogens (Basel, Switzerland) · 2022Review
- TM4SF5-Mediated Regulation of Hepatocyte Transporters during Metabolic Liver Diseases.International journal of molecular sciences · 2022Review
- Virus interactions with the actin cytoskeleton-what we know and do not know about SARS-CoV-2.Archives of virology · 2022Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The hepatitis C virus (HCV) is a major cause of liver diseases ranging from liver inflammation to advanced liver diseases like cirrhosis and hepatocellular carcinoma (HCC). HCV infection is restricted to the liver, and more specifically to hepatocytes, which represent around 80% of liver cells. The mechanism of HCV entry in human hepatocytes has been extensively investigated since the discovery of the virus 30 years ago. The entry mechanism is a multi-step process relying on several host factors including heparan sulfate proteoglycan (HSPG), low density lipoprotein receptor (LDLR), tetraspanin CD81, Scavenger Receptor class B type I (SR-BI), Epidermal Growth Factor Receptor (EGFR) and Niemann-Pick C1-like 1 (NPC1L1). Moreover, in order to establish a persistent infection, HCV entry is dependent on the presence of tight junction (TJ) proteins Claudin-1 (CLDN1) and Occludin (OCLN). In the liver, tight junction proteins play a role in architecture and homeostasis including sealing the apical pole of adjacent cells to form bile canaliculi and separating the basolateral domain drained by sinusoidal blood flow. In this review, we will highlight the role of liver tight junction proteins in HCV infection, and we will discuss the potential targeted therapeutic approaches to improve virus eradication.
Indexed as
Identifiers
What Socratic 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 Socratic graph.