ArticleJournal of virology2014
Increased replicative fitness can lead to decreased drug sensitivity of hepatitis C virus.
Article in Journal of virology, 2014. 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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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.
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Who cites it
51 citing papers in PubMed, 84 citations in OpenAlex.
- Understanding Basic Concepts of Viral Quasispecies: From Evolutionary Dynamics to Clinical Relevance.Pathogens (Basel, Switzerland) · 2026Review
- Synergistic antiviral effects of structure-guided peptides and a mutagenic base analog on SARS-CoV-2 replication.Antimicrobial agents and chemotherapy · 2026Article
- Peaked-to-flat transition in quasispecies structure evolution.Virus evolution · 2026Article
- Viral Quasispecies Inference from Single Observations-Mutagens as Accelerators of Quasispecies Evolution.Microorganisms · 2025Article
- Adapted hepatitis C virus clone infects innate immunity-deficient mouse hepatocytes with minimal human HCV entry factors.JHEP reports : innovation in hepatology · 2025Article
- Association of Liver Damage and Quasispecies Maturity in Chronic HCV Patients: The Fate of a Quasispecies.Microorganisms · 2024Article
- Adapting the rhizome concept to an extended definition of viral quasispecies and the implications for molecular evolution.Scientific reports · 2024Article
- Characterization of virus‒host recombinant variants of the hepatitis E virus.Journal of virology · 2024Article
- Unraveling the dynamics of hepatitis C virus adaptive mutations and their impact on antiviral responses in primary human hepatocytes.Journal of virology · 2024Article
- Unraveling the genomic landscape of piscine myocarditis virus: mutation frequencies, viral diversity and evolutionary dynamics in Atlantic salmon.Virus evolution · 2024Article
- The matrix metalloproteinase ADAM10 supports hepatitis C virus entry and cell-to-cell spread via its sheddase activity.PLoS pathogens · 2023Article
- Substitutions in SARS-CoV-2 Mpro Selected by Protease Inhibitor Boceprevir Confer Resistance to Nirmatrelvir.Viruses · 2023Review
- Fitness-Dependent, Mild Mutagenic Activity of Sofosbuvir for Hepatitis C Virus.Antimicrobial agents and chemotherapy · 2023Article
- Hepatitis C virus fitness can influence the extent of infection-mediated epigenetic modifications in the host cells.Frontiers in cellular and infection microbiology · 2023Article
- In Vitro Susceptibility of HIV Isolates with High Growth Capability to Antiretroviral Drugs.International journal of molecular sciences · 2022Article
- The apparent interferon resistance of transmitted HIV-1 is possibly a consequence of enhanced replicative fitness.PLoS pathogens · 2022Article
- SARS-CoV-2 Mutant Spectra at Different Depth Levels Reveal an Overwhelming Abundance of Low Frequency Mutations.Pathogens (Basel, Switzerland) · 2022Article
- Efficacy decrease of antiviral agents when administered to ongoing hepatitis C virus infections in cell culture.Frontiers in microbiology · 2022Article
- Guanosine inhibits hepatitis C virus replication and increases indel frequencies, associated with altered intracellular nucleotide pools.PLoS pathogens · 2022Article
- A Two-Level, Intramutant Spectrum Haplotype Profile of Hepatitis C Virus Revealed by Self-Organized Maps.Microbiology spectrum · 2021Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
Passage of hepatitis C virus (HCV) in human hepatoma cells resulted in populations that displayed partial resistance to alpha interferon (IFN-α), telaprevir, daclatasvir, cyclosporine, and ribavirin, despite no prior exposure to these drugs. Mutant spectrum analyses and kinetics of virus production in the absence and presence of drugs indicate that resistance is not due to the presence of drug resistance mutations in the mutant spectrum of the initial or passaged populations but to increased replicative fitness acquired during passage. Fitness increases did not alter host factors that lead to shutoff of general host cell protein synthesis and preferential translation of HCV RNA. The results imply that viral replicative fitness is a mechanism of multidrug resistance in HCV. Importance: Viral drug resistance is usually attributed to the presence of amino acid substitutions in the protein targeted by the drug. In the present study with HCV, we show that high viral replicative fitness can confer a general drug resistance phenotype to the virus. The results exclude the possibility that genomes with drug resistance mutations are responsible for the observed phenotype. The fact that replicative fitness can be a determinant of multidrug resistance may explain why the virus is less sensitive to drug treatments in prolonged chronic HCV infections that favor increases in replicative fitness.
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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.