Dynamics of cytotoxic T-lymphocytes and helper cells in human immunodeficiency virus infection with Hill-type infection rate and sigmoidal CTL expansion
DOI10.1016/J.CHAOS.2017.05.036zbMath1375.92026OpenAlexW2620588002MaRDI QIDQ1681651
Nandadulal Bairagi, Debadatta Adak
Publication date: 24 November 2017
Published in: Chaos, Solitons and Fractals (Search for Journal in Brave)
Full work available at URL: https://doi.org/10.1016/j.chaos.2017.05.036
immune systemHIV modelstability switchingCytotoxic T lymphocytes responsegeneralized infection rateself-proliferation
Dynamical systems in biology (37N25) Medical applications (general) (92C50) Qualitative investigation and simulation of ordinary differential equation models (34C60)
Related Items (5)
Cites Work
- Global properties of basic virus dynamics models
- Global properties of a delayed HIV infection model with CTL immune response
- Joint effects of mitosis and intracellular delay on viral dynamics: two-parameter bifurcation analysis
- Critical bifurcations and chaos in a delayed nonlinear model for the immune response
- Global stability of an HIV-1 infection model with saturation infection and intracellular delay
- A delayed HIV-1 infection model with Beddington-DeAngelis functional response
- Global dynamics of a delayed HIV-1 infection model with CTL immune response
- Global dynamics of an in-host viral model with intracellular delay
- Killer cell dynamics. Mathematical and computational approaches to immunology.
- HIV infection and CD\(4^+\) T cell dynamics
- Global stability and periodic solution of the viral dynamics
- Complex dynamic behavior in a viral model with delayed immune response
- Global stability of a deterministic model for HIV infection in vivo
- Dynamical behavior of a delay virus dynamics model with CTL immune response
- Global properties for virus dynamics model with Beddington-DeAngelis functional response
- A delay-differential equation model of HIV infection of \(\text{CD}4^+\) T-cells
- Mathematical analysis of delay differential equation models of HIV-1 infection
- Mathematical modeling of viral kinetics under immune control during primary HIV-1 infection
- Global analysis of HIV-1 dynamics with Hill type infection rate and intracellular delay
- Optimal HIV treatment by maximising immune response
- A model for treatment strategy in the chemotherapy of AIDS
- Analysis of a viral infection model with delayed immune response
- A model of HIV-1 pathogenesis that includes an intracellular delay
- Complex patterns of viral load decay under antiretroviral therapy: influence of pharmacokinetics and intracellular delay
- Some basic properties of immune selection
- Global stability of HIV infection of CD4\(^{+}\) T cells and macrophages with CTL immune response and distributed delays
- Oscillatory viral dynamics in a delayed HIV pathogenesis model
- Global analysis of an epidemic model with nonmonotone incidence rate
- Estimating kinetic parameters from HIV primary infection data through the eyes of three different mathematical models
- Mathematical analysis of the global dynamics of a model for HIV infection of CD4\(^{+}\) T cells
- Study of a system of non-linear difference equations arising in a deterministic model for HIV infection
- Asymptotic properties of a HIV-1 infection model with time delay
- Global Stability of a Nonlinear Viral Infection Model with Infinitely Distributed Intracellular Delays and CTL Immune Responses
- Global stability of pathogen-immune dynamics with absorption
- Virus Dynamics: A Global Analysis
- Immune Responses and Viral Phenotype: Do Replication Rate and Cytopathogenicity Influence Virus Load?
- Impact of Intracellular Delays and Target-Cell Dynamics on In Vivo Viral Infections
- HOW SELF-PROLIFERATION OF CD4+T CELLS AFFECT THE HIV DYNAMICS IN AN IN-HOST TARGET-CELL LIMITED HIV MODEL WITH SATURATION INFECTION RATE: A QUASI-STEADY-STATE APPROXIMATION ANALYSIS
- Global stability of a delayed HIV-1 infection model with absorption and CTL immune response
This page was built for publication: Dynamics of cytotoxic T-lymphocytes and helper cells in human immunodeficiency virus infection with Hill-type infection rate and sigmoidal CTL expansion