ArticlePloS one2016
Lethal Mutagenesis of Hepatitis C Virus Induced by Favipiravir.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
49 citing papers in PubMed.
- Viral Quasispecies Inference from Single Observations-Mutagens as Accelerators of Quasispecies Evolution.Microorganisms · 2025Article
- Quasispecies theory and emerging viruses: challenges and applications.Npj viruses · 2024Review
- Pharmacogenomic Studies of Antiviral Drug Favipiravir.Pharmaceutics · 2024Article
- Favipiravir induces HuNoV viral mutagenesis and infectivity loss with clinical improvement in immunocompromised patients.Clinical immunology (Orlando, Fla.) · 2024Article
- Fitness-Dependent, Mild Mutagenic Activity of Sofosbuvir for Hepatitis C Virus.Antimicrobial agents and chemotherapy · 2023Article
- Favipiravir Suppresses Zika Virus (ZIKV) through Activity as a Mutagen.Microorganisms · 2023Article
- Favipiravir Inhibits Zika Virus (ZIKV) Replication in HeLa Cells by Altering Viral Infectivity.Microorganisms · 2023Article
- Roles of the ACE/Ang II/AT1R pathway, cytokine release, and alteration of tight junctions in COVID-19 pathogenesis.Tissue barriers · 2023Article
- Kill or corrupt: Mechanisms of action and drug-resistance of nucleotide analogues against SARS-CoV-2.Antiviral research · 2023Review
- Atypical Mutational Spectrum of SARS-CoV-2 Replicating in the Presence of Ribavirin.Antimicrobial agents and chemotherapy · 2023Article
- Quasispecies Fitness Partition to Characterize the Molecular Status of a Viral Population. Negative Effect of Early Ribavirin Discontinuation in a Chronically Infected HEV Patient.International journal of molecular sciences · 2022Article
- Potential and action mechanism of favipiravir as an antiviral against Junin virus.PLoS pathogens · 2022Article
- Effects of Drugs Formerly Suggested for COVID-19 Repurposing on Pannexin1 Channels.International journal of molecular sciences · 2022Article
- Review
- SARS-CoV-2 Point Mutation and Deletion Spectra and Their Association with Different Disease Outcomes.Microbiology spectrum · 2022Article
- Lethal Mutagenesis of RNA Viruses and Approved Drugs with Antiviral Mutagenic Activity.Viruses · 2022Review
- Favipiravir Inhibits Hepatitis A Virus Infection in Human Hepatocytes.International journal of molecular sciences · 2022Article
- Efficacy decrease of antiviral agents when administered to ongoing hepatitis C virus infections in cell culture.Frontiers in microbiology · 2022Article
- Enhancing the Antiviral Potency of Nucleobases for Potential Broad-Spectrum Antiviral Therapies.Viruses · 2021Article
- Distinct Antiretroviral Mechanisms Elicited by a Viral Mutagen.Journal of molecular biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Lethal mutagenesis is an antiviral approach that consists in extinguishing a virus by an excess of mutations acquired during replication in the presence of a mutagen. Here we show that favipiravir (T-705) is a potent mutagenic agent for hepatitis C virus (HCV) during its replication in human hepatoma cells. T-705 leads to an excess of G → A and C → U transitions in the mutant spectrum of preextinction HCV populations. Infectivity decreased significantly in the presence of concentrations of T-705 which are 2- to 8-fold lower than its cytotoxic concentration 50 (CC50). Passaging the virus five times in the presence of 400 μM T-705 resulted in virus extinction. Since T-705 has undergone advanced clinical trials for approval for human use, the results open a new approach based on lethal mutagenesis to treat hepatitis C virus infections. If proven effective for HCV in vivo, this new anti-HCV agent may be useful in patient groups that fail current therapeutic regimens.
Indexed as
Identifiers
What OpenQuestion holds
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.