ArticleGastroenterology2009
A mathematical model of hepatitis C virus dynamics in patients with high baseline viral loads or advanced liver disease.
Article in Gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Meta-analysis of hepatitis C virus vaccine efficacy in chimpanzees indicates an importance for structural proteins.Gastroenterology · 2010Pooled it
- Hepatitis C viral kinetics with the nucleoside polymerase inhibitor mericitabine (RG7128).Hepatology (Baltimore, Md.) · 2012Trial
- INHERITANCE OF INTRACELLULAR VIRAL RNA IN A MULTISCALE MODEL OF HEPATITIS C INFECTION.SIAM journal on applied mathematics · 2026Article
- Designing a novel radial basis neural structure for solving the dynamical hepatitis C virus model.Scientific reports · 2025Article
- Modelling HDV kinetics under the entry inhibitor bulevirtide suggests the existence of two HDV-infected cell populations.JHEP reports : innovation in hepatology · 2024Article
- Therapeutic interfering particles exploiting viral replication and assembly mechanisms show promising performance: a modelling study.Scientific reports · 2021Article
- Fuzzy logic and Lyapunov-based non-linear controllers for HCV infection.IET systems biology · 2021Article
- Quantitative differences between intra-host HCV populations from persons with recently established and persistent infections.Virus evolution · 2021Article
- Efficient Methods for Parameter Estimation of Ordinary and Partial Differential Equation Models of Viral Hepatitis Kinetics.Mathematics (Basel, Switzerland) · 2020Article
- Optimal control strategies for preventing hepatitis B infection and reducing chronic liver cirrhosis incidence.Infectious Disease Modelling · 2020Article
- A Parameter Estimation Method for Multiscale Models of Hepatitis C Virus Dynamics.Bulletin of mathematical biology · 2019Article
- Mutational pathway maps and founder effects define the within-host spectrum of hepatitis C virus mutants resistant to drugs.PLoS pathogens · 2019Article
- Modeling suggests that microliter volumes of contaminated blood caused an outbreak of hepatitis C during computerized tomography.PloS one · 2019Article
- Numerical schemes for solving and optimizing multiscale models with age of hepatitis C virus dynamics.Mathematical biosciences · 2018Article
- The Role of Infected Cell Proliferation in the Clearance of Acute HBV Infection in Humans.Viruses · 2017Article
- A Robust and Efficient Numerical Method for RNA-Mediated Viral Dynamics.Frontiers in applied mathematics and statistics · 2017Article
- Estimating biologically relevant parameters under uncertainty for experimental within-host murine West Nile virus infection.Journal of the Royal Society, Interface · 2016Article
- Article
- Severity of liver disease affects HCV kinetics in patients treated with intravenous silibinin monotherapy.Antiviral therapy · 2015Article
- On the laws of virus spread through cell populations.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsPatients with baseline hepatitis C virus-RNA levels (bHCV-RNA)>6 log IU/mL or cirrhosis have a reduced probability of a sustained-virologic response (SVR). We examined the relation between bHCV-RNA, cirrhosis, and SVR with a mathematical model that includes the critical-drug efficacy (epsilonc; the efficacy required for a drug to clear HCV), the infection-rate constant (beta), and the percentage of HCV-infected hepatocytes (pi).
methodsThe relation between baseline factors and SVR was evaluated in 1000 in silico HCV-infected patients, generated by random assignment of realistic host and viral kinetic parameters. Model predictions were compared with clinical data from 170 noncirrhotic and 75 cirrhotic patients.
resultsThe ranges chosen for beta and the viral production rate (p) resulted in bHCV-RNA levels that were in agreement with the distribution observed in US patients. With these beta and p values, higher bHCV-RNA levels led to higher epsilonc, resulting in lower SVR rates. However, higher beta values resulted in lower bHCV-RNA levels but higher pi and (epsilonc), predicting lower rates of SVR. Cirrhotic patients had lower bHCV-RNA levels than noncirrhotic patients (P=.013), and more had bHCV-RNA levels<6 log IU/mL (P<.001). Even cirrhotic patients with lower bHCV-RNA levels had lower SVR rates. An increase in beta could explain the results observed in cirrhotic patients.
conclusionsOur model predicts that higher bHCV-RNA levels lead to higher epsilonc, reducing the chance of achieving SVR; cirrhotic patients have lower SVR rates because of large pi values, caused by increased rates of hepatocyte infection.
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