ArticleBulletin of mathematical biology2012
Modeling quasispecies and drug resistance in hepatitis C patients treated with a protease inhibitor.
Article in Bulletin of mathematical biology, 2012. 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, 42 citations in OpenAlex.
- Naturally occurring dominant drug resistance mutations occur infrequently in the setting of recently acquired hepatitis C.Antiviral therapy · 2015Trial
- Modeling two-strain competition with reinfection: Mathematical analyses and epidemiological implications.Infectious Disease Modelling · 2026Article
- Bifurcation and chaos design of radial basis neural network for predictive modeling of fractional double-strain HIV co-infection model with intercellular delays and stochastic effects.Theory in biosciences = Theorie in den Biowissenschaften · 2026Article
- An Increase in the Prevalence of Clinically Relevant Resistance-Associated Substitutions in Four Direct-Acting Antiviral Regimens: A Study Using GenBank HCV Sequences.Pathogens (Basel, Switzerland) · 2024Article
- Modeling the XBB strain of SARS-CoV-2: Competition between variants and impact of reinfection.Journal of theoretical biology · 2023Article
- A multi-strain model with asymptomatic transmission: Application to COVID-19 in the US.Journal of theoretical biology · 2023Article
- Model-Informed Drug Development for Anti-Infectives: State of the Art and Future.Clinical pharmacology and therapeutics · 2021Review
- Mutational pathway maps and founder effects define the within-host spectrum of hepatitis C virus mutants resistant to drugs.PLoS pathogens · 2019Article
- Virological and Immunological Outcomes of Coinfections.Clinical microbiology reviews · 2018Review
- Interferon at the cellular, individual, and population level in hepatitis C virus infection: Its role in the interferon-free treatment era.Immunological reviews · 2018Review
- Modelling how responsiveness to interferon improves interferon-free treatment of hepatitis C virus infection.PLoS computational biology · 2018Article
- The antigenic variability of HCV in viral HLA-Ag binding is related to the activation of the host immune response.Scientific reports · 2017Article
- Article
- Modelling hepatitis C therapy--predicting effects of treatment.Nature reviews. Gastroenterology & hepatology · 2015Review
- HCV Kinetic Models and Their Implications in Drug Development.CPT: pharmacometrics & systems pharmacology · 2015Review
- Viral kinetic modeling: state of the art.Journal of pharmacokinetics and pharmacodynamics · 2014Review
- Treatment of hepatitis C with an interferon-based lead-in phase: a perspective from mathematical modelling.Antiviral therapy · 2014Article
- A new stochastic model for subgenomic hepatitis C virus replication considers drug resistant mutants.PloS one · 2014Article
- Mathematical analysis of multiscale models for hepatitis C virus dynamics under therapy with direct-acting antiviral agents.Mathematical biosciences · 2013Article
- Combinations of lambda interferon with direct-acting antiviral agents are highly efficient in suppressing hepatitis C virus replication.Antimicrobial agents and chemotherapy · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Telaprevir, a novel hepatitis C virus (HCV) NS3-4A serine protease inhibitor, has demonstrated substantial antiviral activity in patients infected with HCV. However, drug-resistant HCV variants were detected in vivo at relatively high frequency a few days after drug administration. Here we use a two-strain mathematical model to explain the rapid emergence of drug resistance in HCV patients treated with telaprevir monotherapy. We examine the effects of backward mutation and liver cell proliferation on the preexistence of the mutant virus and the competition between wild-type and drug-resistant virus during therapy. We also extend the two-strain model to a general model with multiple viral strains. Mutations during therapy only have a minor effect on the dynamics of various viral strains, although they are capable of generating low levels of HCV variants that would otherwise be completely suppressed because of fitness disadvantages. Liver cell proliferation may not affect the pretreatment frequency of mutant variants, but is able to influence the quasispecies dynamics during therapy. It is the relative fitness of each mutant strain compared with wild-type that determines which strain(s) will dominate the virus population. This study provides a theoretical framework for exploring the prevalence of preexisting mutant variants and the evolution of drug resistance during treatment with other HCV protease inhibitors or polymerase inhibitors.
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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.