ArticleJournal of virology2011
Novel mutations in a tissue culture-adapted hepatitis C virus strain improve infectious-virus stability and markedly enhance infection kinetics.
Article in Journal of virology, 2011. 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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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Novel mutation N588 residue in the NS1 protein of feline parvovirus greatly augments viral replication.Journal of virology · 2024Article
- A Library of Infectious Hepatitis C Viruses with Engineered Mutations in the E2 Gene Reveals Growth-Adaptive Mutations That Modulate Interactions with Scavenger Receptor Class B Type I.Journal of virology · 2016Article
- Cell-death-inducing DFFA-like Effector B Contributes to the Assembly of Hepatitis C Virus (HCV) Particles and Interacts with HCV NS5A.Scientific reports · 2016Article
- Cooperation between the Hepatitis C Virus p7 and NS5B Proteins Enhances Virion Infectivity.Journal of virology · 2015Article
- Adaptive Mutations Enhance Assembly and Cell-to-Cell Transmission of a High-Titer Hepatitis C Virus Genotype 5a Core-NS2 JFH1-Based Recombinant.Journal of virology · 2015Article
- Endoplasmic reticulum stress links hepatitis C virus RNA replication to wild-type PGC-1α/liver-specific PGC-1α upregulation.Journal of virology · 2014Article
- Production and characterization of high-titer serum-free cell culture grown hepatitis C virus particles of genotype 1-6.Virology · 2014Article
- Genetic complementation of hepatitis C virus nonstructural protein functions associated with replication exhibits requirements that differ from those for virion assembly.Journal of virology · 2014Article
- A small-molecule inhibitor of hepatitis C virus infectivity.Antimicrobial agents and chemotherapy · 2014Article
- Preclinical characterization of the novel hepatitis C virus NS3 protease inhibitor GS-9451.Antimicrobial agents and chemotherapy · 2014Article
- Inhibition of hepatitis C virus replication by GS-6620, a potent C-nucleoside monophosphate prodrug.Antimicrobial agents and chemotherapy · 2014Article
- Different responses of two highly permissive cell lines upon HCV infection.Virologica Sinica · 2013Article
- Response of hepatitis C virus to long-term passage in the presence of alpha interferon: multiple mutations and a common phenotype.Journal of virology · 2013Article
- Genetic and functional characterization of the N-terminal region of the hepatitis C virus NS2 protein.Journal of virology · 2013Article
- Permissivity of primary human hepatocytes and different hepatoma cell lines to cell culture adapted hepatitis C virus.PloS one · 2013Article
- Hepatitis C viral entry inhibitors prolong viral suppression by replication inhibitors in persistently-infected Huh7 cultures.PloS one · 2013Article
- Cell culture-adaptive mutations promote viral protein-protein interactions and morphogenesis of infectious hepatitis C virus.Journal of virology · 2012Article
- Viral quasispecies evolution.Microbiology and molecular biology reviews : MMBR · 2012Review
- Cellular growth kinetics distinguish a cyclophilin inhibitor from an HSP90 inhibitor as a selective inhibitor of hepatitis C virus.PloS one · 2012Article
- A genetic interaction between the core and NS3 proteins of hepatitis C virus is essential for production of infectious virus.Journal of virology · 2011Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) establishes persistent infections and leads to chronic liver disease. It only recently became possible to study the entire HCV life cycle due to the ability of a unique cloned patient isolate (JFH-1) to produce infectious particles in tissue culture. However, despite efficient RNA replication, yields of infectious virus particles remain modest. This presents a challenge for large-scale tissue culture efforts, such as inhibitor screening. Starting with a J6/JFH-1 chimeric virus, we used serial passaging to generate a virus with substantially enhanced infectivity and faster infection kinetics compared to the parental stock. The selected virus clone possessed seven novel amino acid mutations. We analyzed the contribution of individual mutations and identified three specific mutations, core K78E, NS2 W879R, and NS4B V1761L, which were necessary and sufficient for the adapted phenotype. These three mutations conferred a 100-fold increase in specific infectivity compared to the parental J6/JFH-1 virus, and media collected from cells infected with the adapted virus yielded infectious titers as high as 1 × 10(8) 50% tissue culture infective doses (TCID(50))/ml. Further analyses indicated that the adapted virus has longer infectious stability at 37°C than the wild type. Given that the adapted phenotype resulted from a combination of mutations in structural and nonstructural proteins, these data suggest that the improved viral titers are likely due to differences in virus particle assembly that result in significantly improved infectious particle stability. This adapted virus will facilitate further studies of the HCV life cycle, virus structure, and high-throughput drug screening.
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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.