ArticlePLoS pathogens2010
Adaptation of hepatitis C virus to mouse CD81 permits infection of mouse cells in the absence of human entry factors.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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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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Who cites it
71 citing papers in PubMed, 112 citations in OpenAlex.
- O'nyong-nyong virus adaptive mutations in non-structural protein 1 and 3 enhance RNA replication and overcome FHL1 requirement.Emerging microbes & infections · 2026Article
- Assessment of hepatitis C virus permissiveness in iteratively genetically humanized mice.Journal of virology · 2025Article
- Adapted hepatitis C virus clone infects innate immunity-deficient mouse hepatocytes with minimal human HCV entry factors.JHEP reports : innovation in hepatology · 2025Article
- The triglyceride-synthesizing enzyme diacylglycerol acyltransferase 2 modulates the formation of the hepatitis C virus replication organelle.PLoS pathogens · 2024Article
- Unraveling the dynamics of hepatitis C virus adaptive mutations and their impact on antiviral responses in primary human hepatocytes.Journal of virology · 2024Article
- Marmosets as models of infectious diseases.Frontiers in cellular and infection microbiology · 2024Review
- Packaging defects in pestiviral NS4A can be compensated by mutations in NS2 and NS3.Journal of virology · 2023Article
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- Characterization of RNA Sensing Pathways in Hepatoma Cell Lines and Primary Human Hepatocytes.Cells · 2021Article
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- Interdependent Impact of Lipoprotein Receptors and Lipid-Lowering Drugs on HCV Infectivity.Cells · 2021Article
- Cholesterol sensing by CD81 is important for hepatitis C virus entry.The Journal of biological chemistry · 2020Article
- P108 and T109 on E2 Glycoprotein Domain I Are Critical for the Adaptation of Classical Swine Fever Virus to Rabbits but Not for Virulence in Pigs.Journal of virology · 2020Article
- Single-nucleotide variants in human CD81 influence hepatitis C virus infection of hepatoma cells.Medical microbiology and immunology · 2020Article
- Host-Directed Antiviral Therapy.Clinical microbiology reviews · 2020Review
- The ATGL lipase cooperates with ABHD5 to mobilize lipids for hepatitis C virus assembly.PLoS pathogens · 2020Article
- Animal Models Used in Hepatitis C Virus Research.International journal of molecular sciences · 2020Review
- Animal Models of Hepatitis C Virus Infection.Cold Spring Harbor perspectives in medicine · 2020Review
- Differences across cyclophilin A orthologs contribute to the host range restriction of hepatitis C virus.eLife · 2019Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) naturally infects only humans and chimpanzees. The determinants responsible for this narrow species tropism are not well defined. Virus cell entry involves human scavenger receptor class B type I (SR-BI), CD81, claudin-1 and occludin. Among these, at least CD81 and occludin are utilized in a highly species-specific fashion, thus contributing to the narrow host range of HCV. We adapted HCV to mouse CD81 and identified three envelope glycoprotein mutations which together enhance infection of cells with mouse or other rodent receptors approximately 100-fold. These mutations enhanced interaction with human CD81 and increased exposure of the binding site for CD81 on the surface of virus particles. These changes were accompanied by augmented susceptibility of adapted HCV to neutralization by E2-specific antibodies indicative of major conformational changes of virus-resident E1/E2-complexes. Neutralization with CD81, SR-BI- and claudin-1-specific antibodies and knock down of occludin expression by siRNAs indicate that the adapted virus remains dependent on these host factors but apparently utilizes CD81, SR-BI and occludin with increased efficiency. Importantly, adapted E1/E2 complexes mediate HCV cell entry into mouse cells in the absence of human entry factors. These results further our knowledge of HCV receptor interactions and indicate that three glycoprotein mutations are sufficient to overcome the species-specific restriction of HCV cell entry into mouse cells. Moreover, these findings should contribute to the development of an immunocompetent small animal model fully permissive to HCV.
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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.