ArticleHepatology (Baltimore, Md.)2011
Expression of paramyxovirus V proteins promotes replication and spread of hepatitis C virus in cultures of primary human fetal liver cells.
Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 84 citations in OpenAlex.
- Bioprinted platform for parallelized screening of engineered microtissues in vivo.Cell stem cell · 2025Article
- Molecular biology of canine parainfluenza virus V protein and its potential applications in tumor immunotherapy.Frontiers in microbiology · 2023Review
- Initial HCV infection of adult hepatocytes triggers a temporally structured transcriptional program containing diverse pro- and anti-viral elements.Journal of virology · 2021Article
- Engineering andMolecular therapy. Methods & clinical development · 2020Article
- Equine pegiviruses cause persistent infection of bone marrow and are not associated with hepatitis.PLoS pathogens · 2020Article
- Article
- Expansion, in vivo-ex vivo cycling, and genetic manipulation of primary human hepatocytes.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Hepatitis B Virus-Hepatocyte Interactions and Innate Immune Responses: Experimental Models and Molecular Mechanisms.Seminars in liver disease · 2019Review
- Multivascular networks and functional intravascular topologies within biocompatible hydrogels.Science (New York, N.Y.) · 2019Article
- Mononuclear phagocyte system in hepatitis C virus infection.World journal of gastroenterology · 2018Review
- Pan-Genotype Hepatitis E Virus Replication in Stem Cell-Derived Hepatocellular Systems.Gastroenterology · 2018Article
- Manipulation of both virus- and cell-specific factors is required for robust transient replication of a hepatitis C virus genotype 3a sub-genomic replicon.The Journal of general virology · 2017Article
- Tumor Necrosis Factor Inhibits Spread of Hepatitis C Virus Among Liver Cells, Independent From Interferons.Gastroenterology · 2017Article
- The IFN-λ-IFN-λR1-IL-10Rβ Complex Reveals Structural Features Underlying Type III IFN Functional Plasticity.Immunity · 2017Article
- Innate and Adaptive Immune Responses in Chronic HCV Infection.Current drug targets · 2017Review
- Humanized mice efficiently engrafted with fetal hepatoblasts and syngeneic immune cells develop human monocytes and NK cells.Journal of hepatology · 2016Article
- Viral genome imaging of hepatitis C virus to probe heterogeneous viral infection and responses to antiviral therapies.Virology · 2016Article
- Experimental models of hepatitis B and C - new insights and progress.Nature reviews. Gastroenterology & hepatology · 2016Review
- Superior In vivo Transduction of Human Hepatocytes Using Engineered AAV3 Capsid.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Proteomics of HCV virions reveals an essential role for the nucleoporin Nup98 in virus morphogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
unlabelledHere we demonstrate that primary cultures of human fetal liver cells (HFLC) reliably support infection with laboratory strains of hepatitis C virus (HCV), although levels of virus replication vary significantly between different donor cell preparations and frequently decline in a manner suggestive of active viral clearance. To investigate possible contributions of the interferon (IFN) system to control HCV infection in HFLC, we exploited the well-characterized ability of paramyxovirus (PMV) V proteins to counteract both IFN induction and antiviral signaling. The V proteins of measles virus (MV) and parainfluenza virus 5 (PIV5) were introduced into HFLC using lentiviral vectors encoding a fluorescent reporter for visualization of HCV-infected cells. V protein-transduced HFLC supported enhanced (10 to 100-fold) levels of HCV infection relative to untransduced or control vector-transduced HFLC. Infection was assessed by measurement of virus-driven luciferase, by assays for infectious HCV and viral RNA, and by direct visualization of HCV-infected hepatocytes. Live cell imaging between 48 and 119 hours postinfection demonstrated little or no spread of infection in the absence of PMV V protein expression. In contrast, V protein-transduced HFLC showed numerous HCV infection events. V protein expression efficiently antagonized the HCV-inhibitory effects of added IFNs in HFLC. In addition, induction of the type III IFN, IL29, following acute HCV infection was inhibited in V protein-transduced cultures.
conclusionThese studies suggest that the cellular IFN response plays a significant role in limiting the spread of HCV infection in primary hepatocyte cultures. Strategies aimed at dampening this response may be key to further development of robust HCV culture systems, enabling studies of virus pathogenicity and the mechanisms by which HCV spreads in its natural host cell population.
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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.