scholarly journals Global Dynamics of a Delayed HIV-1 Infection Model with CTL Immune Response

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Yunfei Li ◽  
Rui Xu ◽  
Zhe Li ◽  
Shuxue Mao

A delayed HIV-1 infection model with CTL immune response is investigated. By using suitable Lyapunov functionals, it is proved that the infection-free equilibrium is globally asymptotically stable if the basic reproduction ratio for viral infection is less than or equal to unity; if the basic reproduction ratio for CTL immune response is less than or equal to unity and the basic reproduction ratio for viral infection is greater than unity, the CTL-inactivated infection equilibrium is globally asymptotically stable; if the basic reproduction ratio for CTL immune response is greater than unity, the CTL-activated infection equilibrium is globally asymptotically stable.

2013 ◽  
Vol 2013 ◽  
pp. 1-12
Author(s):  
Haibin Wang ◽  
Rui Xu

An HIV-1 infection model with latently infected cells and delayed immune response is investigated. By analyzing the corresponding characteristic equations, the local stability of each of feasible equilibria is established and the existence of Hopf bifurcations at the CTL-activated infection equilibrium is also studied. By means of suitable Lyapunov functionals and LaSalle’s invariance principle, it is proved that the infection-free equilibrium is globally asymptotically stable if the basic reproduction ratio for viral infectionR0≤1; if the basic reproduction ratio for viral infectionR0>1and the basic reproduction ratio for CTL immune responseR1≤1, the CTL-inactivated infection equilibrium is globally asymptotically stable. If the basic reproduction ratio for CTL immune responseR1>1, the global stability of the CTL-activated infection equilibrium is also derived when the time delayτ=0. Numerical simulations are carried out to illustrate the main results.


2012 ◽  
Vol 05 (03) ◽  
pp. 1260012 ◽  
Author(s):  
RUI XU

In this paper, an HIV-1 infection model with absorption, saturation infection and an intracellular delay accounting for the time between viral entry into a target cell and the production of new virus particles is investigated. By analyzing the characteristic equations, the local stability of an infection-free equilibrium and a chronic-infection equilibrium of the model is established. By using suitable Lyapunov functionals and LaSalle's invariance principle, it is proved that if the basic reproduction ratio is less than unity, the infection-free equilibrium is globally asymptotically stable; and if the basic reproduction ratio is greater than unity, sufficient condition is derived for the global stability of the chronic-infection equilibrium.


2021 ◽  
Vol 26 (1) ◽  
pp. 1-20
Author(s):  
Chenwei Song ◽  
Rui Xu

In this paper, we consider an improved Human T-lymphotropic virus type I (HTLV-I) infection model with the mitosis of CD4+ T cells and delayed cytotoxic T-lymphocyte (CTL) immune response by analyzing the distributions of roots of the corresponding characteristic equations, the local stability of the infection-free equilibrium, the immunity-inactivated equilibrium, and the immunity-activated equilibrium when the CTL immune delay is zero is established. And we discuss the existence of Hopf bifurcation at the immunity-activated equilibrium. We define the immune-inactivated reproduction ratio R0 and the immune-activated reproduction ratio R1. By using Lyapunov functionals and LaSalle’s invariance principle, it is shown that if R0 < 1, the infection-free equilibrium is globally asymptotically stable; if R1 < 1 < R0, the immunity-inactivated equilibrium is globally asymptotically stable; if R1 > 1, the immunity-activated equilibrium is globally asymptotically stable when the CTL immune delay is zero. Besides, uniform persistence is obtained when R1 > 1. Numerical simulations are carried out to illustrate the theoretical results.


2017 ◽  
Vol 10 (05) ◽  
pp. 1750070 ◽  
Author(s):  
A. M. Ełaiw ◽  
A. A. Raezah ◽  
Khalid Hattaf

This paper studies the dynamical behavior of an HIV-1 infection model with saturated virus-target and infected-target incidences with Cytotoxic T Lymphocyte (CTL) immune response. The model is incorporated by two types of intracellular distributed time delays. The model generalizes all the existing HIV-1 infection models with cell-to-cell transmission presented in the literature by considering saturated incidence rate and the effect of CTL immune response. The existence and global stability of all steady states of the model are determined by two parameters, the basic reproduction number ([Formula: see text]) and the CTL immune response activation number ([Formula: see text]). By using suitable Lyapunov functionals, we show that if [Formula: see text], then the infection-free steady state [Formula: see text] is globally asymptotically stable; if [Formula: see text] [Formula: see text], then the CTL-inactivated infection steady state [Formula: see text] is globally asymptotically stable; if [Formula: see text], then the CTL-activated infection steady state [Formula: see text] is globally asymptotically stable. Using MATLAB we conduct some numerical simulations to confirm our results. The effect of the saturated incidence of the HIV-1 dynamics is shown.


2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Hui Miao ◽  
Xamxinur Abdurahman ◽  
Ahmadjan Muhammadhaji

We investigate global dynamics for a system of delay differential equations which describes a virus-immune interaction in vivo. The model has two time delays describing time needed for infection of cell and CTLs generation. Our model admits three possible equilibria: infection-free equilibrium, CTL-absent infection equilibrium, and CTL-present infection equilibrium. The effect of time delay on stability of the equilibria of the CTL immune response model has been studied.


2016 ◽  
Vol 10 (01) ◽  
pp. 1750012 ◽  
Author(s):  
Lijuan Song ◽  
Cui Ma ◽  
Qiang Li ◽  
Aijun Fan ◽  
Kaifa Wang

In this paper, mathematical analysis of the global dynamics of a viral infection model in vivo is carried out. Though the model is originally to study hepatitis C virus (HCV) dynamics in patients with high baseline viral loads or advanced liver disease, similar models still hold significance for other viral infection, such as hepatitis B virus (HBV) or human immunodeficiency virus (HIV) infection. By means of Volterra-type Lyapunov functions, we know that the basic reproduction number [Formula: see text] is a sharp threshold para-meter for the outcomes of viral infections. If [Formula: see text], the virus-free equilibrium is globally asymptotically stable. If [Formula: see text], the system is uniformly persistent, the unique endemic equilibrium appears and is globally asymptotically stable under a sufficient condition. Other than that, for the global stability of the unique endemic equilibrium, another sufficient condition is obtained by Li–Muldowney global-stability criterion. Using numerical simulation techniques, we further find that sustained oscillations can exist and different maximum de novo hepatocyte influx rate can induce different global dynamics along with the change of overall drug effectiveness. Finally, some biological implications of our findings are given.


2012 ◽  
Vol 05 (06) ◽  
pp. 1250058 ◽  
Author(s):  
SHIFEI WANG ◽  
YICANG ZHOU

In this paper, we investigate global dynamics for an in-host HIV-1 infection model with the long-lived infected cells and four intracellular delays. Our model admits two possible equilibria, an uninfected equilibrium and infected equilibrium depending on the basic reproduction number. We derive that the global dynamics are completely determined by the values of the basic reproduction number: if the basic reproduction number is less than one, the uninfected equilibrium is globally asymptotically stable, and the virus is cleared; if the basic reproduction number is larger than one, then the infection persists, and the infected equilibrium is globally asymptotically stable.


2019 ◽  
Vol 27 (01) ◽  
pp. 19-49 ◽  
Author(s):  
BAKARY TRAORÉ ◽  
OUSMANE KOUTOU ◽  
BOUREIMA SANGARÉ

In this paper, we investigate a nonautonomous and an autonomous model of schistosomiasis transmission with a general incidence function. Firstly, we formulate the nonautonomous model by taking into account the effect of climate change on the transmission. Through rigorous analysis via theories and methods of dynamical systems, we show that the nonautonomous model has a globally asymptotically stable disease-free periodic equilibrium when the associated basic reproduction ratio [Formula: see text] is less than unity. Otherwise, the system admits at least one positive periodic solutions if [Formula: see text] is greater than unity. Secondly, using the average of periodic functions, we further derive the autonomous model associated with the nonautonomous model. Therefore, we show that the disease-free equilibrium of the autonomous model is locally and globally asymptotically stable when the associated reproduction ratio [Formula: see text] is less than unity. When [Formula: see text] is greater than unity, the existence and global asymptotic stability of the endemic equilibrium is established under certain conditions. Finally, using linear and nonlinear specific incidence function, we perform some numerical simulations to illustrate our theoretical results.


2015 ◽  
Vol 2015 ◽  
pp. 1-11
Author(s):  
Xinxin Tian ◽  
Jinliang Wang

We formulate a (2n+2)-dimensional viral infection model with humoral immunity,nclasses of uninfected target cells and  nclasses of infected cells. The incidence rate of infection is given by nonlinear incidence rate, Beddington-DeAngelis functional response. The model admits discrete time delays describing the time needed for infection of uninfected target cells and virus replication. By constructing suitable Lyapunov functionals, we establish that the global dynamics are determined by two sharp threshold parameters:R0andR1. Namely, a typical two-threshold scenario is shown. IfR0≤1, the infection-free equilibriumP0is globally asymptotically stable, and the viruses are cleared. IfR1≤1<R0, the immune-free equilibriumP1is globally asymptotically stable, and the infection becomes chronic but with no persistent antibody immune response. IfR1>1, the endemic equilibriumP2is globally asymptotically stable, and the infection is chronic with persistent antibody immune response.


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