ArticleJournal of virology2013
Evasion of superinfection exclusion and elimination of primary viral RNA by an adapted strain of hepatitis C virus.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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
25 citing papers in PubMed, 48 citations in OpenAlex.
- Double trouble: how co- and superinfections shape viral dynamics and host responses.Journal of virology · 2026Review
- Rethinking viral evolution: How BIAS mechanisms and Gamma-Poisson overdispersion redefine lethal mutagenesis.Frontiers in microbiology · 2026Article
- Japanese encephalitis virus inhibits superinfection of Zika virus in cells by the NS2B protein.Journal of virology · 2024Article
- Mimicking superinfection exclusion disrupts alphavirus infection and transmission in the yellow fever mosquitoProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Virus-induced interference as a means for accelerating fitness-based selection of cyprinid herpesvirus 3 single-nucleotide variantsVirus evolution · 2023Article
- Killing the competition: a theoretical framework for liver-stage malaria.Open biology · 2022Article
- Article
- Regulation of the Transferrin Receptor Recycling in Hepatitis C Virus-Replicating Cells.Frontiers in cell and developmental biology · 2020Article
- Mutational pathway maps and founder effects define the within-host spectrum of hepatitis C virus mutants resistant to drugs.PLoS pathogens · 2019Article
- HCV transmission in high-risk communities in Bulgaria.PloS one · 2019Article
- Superinfection and cure of infected cells as mechanisms for hepatitis C virus adaptation and persistence.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- QUENTIN: reconstruction of disease transmissions from viral quasispecies genomic data.Bioinformatics (Oxford, England) · 2018Article
- A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion.Frontiers in plant science · 2018Review
- Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis.Journal of visualized experiments : JoVE · 2017Article
- A self-perpetuating repressive state of a viral replication protein blocks superinfection by the same virus.PLoS pathogens · 2017Article
- The Coat Protein and NIa Protease of Two Potyviridae Family Members Independently Confer Superinfection Exclusion.Journal of virology · 2016Article
- Hepatitis C Virus RNA-Dependent RNA Polymerase Interacts with the Akt/PKB Kinase and Induces Its Subcellular Relocalization.Antimicrobial agents and chemotherapy · 2016Article
- Antagonistic within-host interactions between plant viruses: molecular basis and impact on viral and host fitness.Molecular plant pathology · 2016Review
- Article
- Modelling hepatitis C therapy--predicting effects of treatment.Nature reviews. Gastroenterology & hepatology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cells that are productively infected by hepatitis C virus (HCV) are refractory to a second infection by HCV via a block in viral replication known as superinfection exclusion. The block occurs at a postentry step and likely involves translation or replication of the secondary viral RNA, but the mechanism is largely unknown. To characterize HCV superinfection exclusion, we selected for an HCV variant that could overcome the block. We produced a high-titer HC-J6/JFH1 (Jc1) viral genome with a fluorescent reporter inserted between NS5A and NS5B and used it to infect Huh7.5 cells containing a Jc1 replicon. With multiple passages of these infected cells, we isolated an HCV variant that can superinfect cells at high levels. Notably, the superinfectious virus rapidly cleared the primary replicon from superinfected cells. Viral competition experiments, using a novel strategy of sequence-barcoding viral strains, as well as superinfection of replicon cells demonstrated that mutations in E1, p7, NS5A, and the poly(U/UC) tract of the 3' untranslated region were important for superinfection. Furthermore, these mutations dramatically increased the infectivity of the virus in naive cells. Interestingly, viruses with a shorter poly(U/UC) and an NS5A domain II mutation were most effective in overcoming the postentry block. Neither of these changes affected viral RNA translation, indicating that the major barrier to postentry exclusion occurs at viral RNA replication. The evolution of the ability to superinfect after less than a month in culture and the concomitant exclusion of the primary replicon suggest that superinfection exclusion dramatically affects viral fitness and dynamics in vivo.
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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 OpenQuestion graph.