ArticleJournal of mathematical biology2010
Rich dynamics of a hepatitis B viral infection model with logistic hepatocyte growth.
Article in Journal of mathematical biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Survey on mathematical modeling of infectious disease dynamics: insights and applications.BMC infectious diseases · 2026Review
- A Quantitative Systems Pharmacology (QSP) Model of Acute Hepatitis B Virus Infection: Mechanistic Insights and Foundations for Future Extensions.CPT: pharmacometrics & systems pharmacology · 2026Article
- Investigation of a Two-Patch Within-Host Model of Hepatitis B Viral Infection.Bulletin of mathematical biology · 2025Article
- Disease Progression Mathematical Modeling With a Case Study on Hepatitis B Virus Infection.CPT: pharmacometrics & systems pharmacology · 2025Review
- Dynamical analysis of a general delayed HBV infection model with capsids and adaptive immune response in presence of exposed infected hepatocytes.Journal of mathematical biology · 2024Article
- Viral Infection Model with Diffusion and Distributed Delay: Finite-Dimensional Global Attractor.Qualitative theory of dynamical systems · 2023Article
- Aerosol Transport Modeling: The Key Link Between Lung Infections of Individuals and Populations.Frontiers in physiology · 2022Review
- An Explainable Artificial Intelligence Framework for the Deterioration Risk Prediction of Hepatitis Patients.Journal of medical systems · 2021Article
- Understanding the antiviral effects of RNAi-based therapy in HBeAg-positive chronic hepatitis B infection.Scientific reports · 2021Article
- Acute hepatitis B virus infection model within the host incorporating immune cells and cytokine responses.Theory in biosciences = Theorie in den Biowissenschaften · 2020Article
- Impact of Population Recruitment on the HIV Epidemics and the Effectiveness of HIV Prevention Interventions.Bulletin of mathematical biology · 2016Article
- New insights into the evolutionary rate of hepatitis B virus at different biological scales.Journal of virology · 2015Article
- Analysis and simulation of an Adefovir anti-hepatitis B virus infection therapy immune model with alanine aminotransferase.IET systems biology · 2013Article
- Modeling and simulating dynamics of complete- and poor-response chronic hepatitis B chinese patients for adefovir and traditional chinese medicine plus adefovir therapy.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Modeling the adaptive immune response in HBV infection.Journal of mathematical biology · 2011Article
- Distinct hepatitis B virus dynamics in the immunotolerant and early immunoclearance phases.Journal of virology · 2010Article
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis B virus (HBV) infection is a major cause of human suffering, and a number of mathematical models have examined within-host dynamics of the disease. Most previous HBV infection models have assumed that: (a) hepatocytes regenerate at a constant rate from a source outside the liver; and/or (b) the infection takes place via a mass action process. Assumption (a) contradicts experimental data showing that healthy hepatocytes proliferate at a rate that depends on current liver size relative to some equilibrium mass, while assumption (b) produces a problematic basic reproduction number. Here we replace the constant infusion of healthy hepatocytes with a logistic growth term and the mass action infection term by a standard incidence function; these modifications enrich the dynamics of a well-studied model of HBV pathogenesis. In particular, in addition to disease free and endemic steady states, the system also allows a stable periodic orbit and a steady state at the origin. Since the system is not differentiable at the origin, we use a ratio-dependent transformation to show that there is a region in parameter space where the origin is globally stable. When the basic reproduction number, R (0), is less than 1, the disease free steady state is stable. When R (0) > 1 the system can either converge to the chronic steady state, experience sustained oscillations, or approach the origin. We characterize parameter regions for all three situations, identify a Hopf and a homoclinic bifurcation point, and show how they depend on the basic reproduction number and the intrinsic growth rate of hepatocytes.
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