ArticleJournal of virology2004
In vivo analysis of the 3' untranslated region of GB virus B after in vitro mutagenesis of an infectious cDNA clone: persistent infection in a transfected tamarin.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 38 citations in OpenAlex.
- Marmosets as models of infectious diseases.Frontiers in cellular and infection microbiology · 2024Review
- Clinical and molecular aspects of human pegiviruses in the interaction host and infectious agent.Virology journal · 2022Review
- Animal Models Used in Hepatitis C Virus Research.International journal of molecular sciences · 2020Review
- Viral persistence, liver disease, and host response in a hepatitis C-like virus rat model.Hepatology (Baltimore, Md.) · 2018Article
- Infection of Common Marmosets with GB Virus B Chimeric Virus Encoding the Major Nonstructural Proteins NS2 to NS4A of Hepatitis C Virus.Journal of virology · 2016Article
- Detection of non-primate hepaciviruses in UK dogs.Virology · 2015Article
- Changes in immune cell populations in the periphery and liver of GBV-B-infected and convalescent tamarins (Saguinus labiatus).Virus research · 2014Article
- Modeling HCV disease in animals: virology, immunology and pathogenesis of HCV and GBV-B infections.Frontiers in microbiology · 2014Review
- Serology-enabled discovery of genetically diverse hepaciviruses in a new host.Journal of virology · 2012Article
- Characterization of a canine homolog of hepatitis C virus.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- The GB viruses: a review and proposed classification of GBV-A, GBV-C (HGV), and GBV-D in genus Pegivirus within the family Flaviviridae.The Journal of general virology · 2011Review
- Long-Term Persistent GBV-B Infection and Development of a Chronic and Progressive Hepatitis C-Like Disease in Marmosets.Frontiers in microbiology · 2011Article
- Molecular evolution of GB virus B hepatitis virus during acute resolving and persistent infections in experimentally infected tamarins.The Journal of general virology · 2010Article
- HCV animal models: a journey of more than 30 years.Viruses · 2009Article
- Article
- Lack of adaptation of chimeric GB virus B/hepatitis C virus in the marmoset model: possible effects of bottleneck.Journal of virology · 2009Article
- The marmoset model of GB virus B infections: adaptation to host phenotypic variation.Journal of virology · 2009Article
- Article
- New animal models for hepatitis C viral infection and pathogenesis studies.World journal of gastroenterology · 2007Review
- GB virus B disrupts RIG-I signaling by NS3/4A-mediated cleavage of the adaptor protein MAVS.Journal of virology · 2007Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
GB virus B (GBV-B), the virus most closely related to hepatitis C virus (HCV), infects tamarins and causes acute hepatitis. The 3' untranslated region (UTR) of an infectious GBV-B clone (pGBB) has a proximal short sequence followed by a poly(U) tract and a 3' terminal sequence. Our investigators previously demonstrated that the 3' terminal sequence was critical for in vivo infectivity. Here, we tested the effect of deleting the short sequence and/or the poly(U) tract from pGBB; infectivity of each mutant was tested by intrahepatic transfection of two tamarins with transcribed RNA. A mutant lacking both regions was not viable. However, mutants lacking either the short sequence or the poly(U) tract were viable. All four tamarins had a wild-type-like acute infection and developed acute hepatitis. Whereas we found that five tamarins transfected with the wild-type clone pGBB had acute resolving infection, one tamarin transfected with the poly(U) deletion mutant became persistently infected. This animal had viremia and hepatitis until its death at week 90. The genomes recovered at weeks 2, 7, 15, 20, 60, and 90 lacked the poly(U) stretch. Eight amino acid changes were identified at week 90. One change, in the putative p7 protein, was dominant at week 15. Thus, persistence of GBV-B, like persistence of HCV, was associated with the emergence of virus variants. Four tamarins inoculated with serum collected at weeks 2 and 90 from the tamarin with persistent infection had an acute resolving infection. Nonetheless, the demonstration that GBV-B can persist in tamarins strengthens its relevance as a surrogate model for the study of HCV.
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