Global dynamics of delay‐distributed HIV infection models with differential drug efficacy in cocirculating target cells

In this paper, we investigate the dynamical behaviors of three human immunodeficiency virus infection models with two types of cocirculating target cells and distributed intracellular delay. The models take into account both short‐lived infected cells and long‐lived chronically infected cells. In the two types of target cells, the drug efficacy is assumed to be different. The incidence rate of infection is given by bilinear and saturation functional responses in the first and second models, respectively, while it is given by a general function in the third model. Lyapunov functionals are constructed and LaSalle invariance principle is applied to prove the global asymptotic stability of all equilibria of the models. We have derived the basic reproduction number R₀ for the three models. For the first two models, we have proven that the disease‐free equilibrium is globally asymptotically stable (GAS) when R₀≤1, and the endemic equilibrium is GAS when R₀>1. For the third model, we have established a set of sufficient conditions for global stability of both equilibria of the model. We have checked our theoretical results with numerical simulations. Copyright © 2015 John Wiley & Sons, Ltd.     

Global stability of humoral immunity virus dynamics models with nonlinear infection rate and removal

In this paper, we investigate the dynamical behavior of two nonlinear models for viral infection with humoral immune response. The first model contains four compartments; uninfected target cells, actively infected cells, free virus particles and B cells. The intrinsic growth rate of uninfected cells, incidence rate of infection, removal rate of infected cells, production rate of viruses, neutralization rate of viruses, activation rate of B cells and removal rate of B cells are given by more general nonlinear functions. The second model is a modification of the first one by including an eclipse stage of infected cells. We assume that the latent-to-active conversion rate is also given by a more general nonlinear function. For each model we derive two threshold parameters and establish a set of conditions on the general functions which are sufficient to determine the global dynamics of the models. By using suitable Lyapunov functions and LaSalle’s invariance principle, we prove the global asymptotic stability of the all equilibria of the models. We perform some numerical simulations for the models with specific forms of the general functions and show that the numerical results are consistent with the theoretical results.     

Dynamics of an HIV‐1 virus model with both virus‐to‐cell and cell‐to‐cell transmissions,general incidence rate,intracellular delay,and CTL immune responses

Direct cell‐to‐cell transmission of HIV‐1 is a more efficient means of virus infection than virus‐to‐cell transmission. In this paper, we incorporate both these transmissions into an HIV‐1 virus model with nonlinear general incidence rate, intracellular delay, and cytotoxic T lymphocyte (CTL) immune responses. This model admits three types of equilibria: infection‐free equilibrium, CTL‐inactivated equilibrium, and CTL‐activated equilibrium. By using Lyapunov functionals and LaSalle invariance principle, it is verified that global threshold dynamics of the model can be explicitly described by the basic reproduction numbers.     

Stability of a general adaptive immunity virus dynamics model with multistages of infected cells and two routes of infection

This paper studies an (n+4)-dimensional nonlinear virus dynamics model that characterizes the interactions of the viruses, susceptible host cells, n-stages of infected cells, B cells and cytotoxic T lymphocyte (CTL) cells. Both viral and cellular infections have been incorporated into the model. The infected-susceptible and virus-susceptible infection rates as well as the generation and removal rates of all compartments are described by general nonlinear functions. Five threshold parameters are computed, which insure the existence of the equilibria of the model under consideration. A set of conditions on the general functions has been established, which is sufficient to investigate the global dynamics of the model. The global asymptotic stability of all equilibria is proven by utilizing Lyapunov function and LaSalle's invariance principle. The theoretical results are illustrated by numerical simulations of the model with specific forms of the general functions.     

Global stability of delay-distributed viral infection model with two modes of viral transmission and B-cell impairment

This paper formulates a virus dynamics model with impairment of B-cell functions. The model incorporates two modes of viral transmission: cell-free and cell-to-cell. The cell-free and cell-cell incidence rates are modeled by general functions. The model incorporates both, latently and actively, infected cells as well as three distributed time delays. Nonnegativity and boundedness properties of the solutions are proven to show the well-posedness of the model. The model admits two equilibria that are determined by the basic reproduction number R₀. The global stability of each equilibrium is proven by utilizing Lyapunov function and LaSalle's invariance principle. The theoretical results are illustrated by numerical simulations. The effect of impairment of B-cell functions and time delays on the virus dynamics are studied. We have shown that if the functions of B-cell is impaired, then the concentration of viruses is increased in the plasma. Moreover, we have observed that increasing the time delay will suppress the viral replication.     

Global stability properties of age‐dependent epidemic models with varying rates of recurrence

The purpose of this paper is to study the global stability properties of equilibria for age‐dependent epidemiological models in presence of recurrence phenomenon. In these systems, the recurrence rate depends on asymptomatic–infection–age. The models are appropriate for human herpes virus (HSV‐1 and HSV‐2) and varicella‐zoster virus. We derived explicit formulas for the basic reproductive number, which completely characterizes the global behaviour of solutions to the models: if the basic reproductive number is less than or equal to unity, the disease will die out; if the basic reproductive number is greater than unity, the disease will be persistent. Volterra‐type Lyapunov functions are constructed to establish the global asymptotic stability of the infection‐free and endemic steady states. Copyright © 2015 John Wiley & Sons, Ltd.     

Stability analysis of a virus infection model with humoral immunity response and two time delays

In this paper, we investigate the dynamical properties for a model of delay differential equations, which describes a virus‐immune interaction in vivo. By analyzing corresponding characteristic equations, the local stability of the equilibria for infection‐free, antibody‐free, and antibody response and the existence of Hopf bifurcation with antibody response delay as a bifurcation parameter at the antibody‐activated infection equilibrium are established, respectively. Global stability of the equilibria for infection‐free, antibody‐free, and antibody response, respectively, also are established by applying the Lyapunov functionals method. The numerical simulations are performed in order to illustrate the dynamical behavior of the model. Copyright © 2016 John Wiley & Sons, Ltd.     

Disease‐selective predation may lead to prey extinction

In real world bio‐communities, predational choice plays a key role to the persistence of the prey population. Predator's ‘sense’ of choice for predation towards the infected and noninfected prey is an important factor for those bio‐communities. There are examples where the predator can distinguish the infected prey and avoids those at the time of predation. Based on the examples, we propose two mathematical models and observe the dynamics of the systems around biologically feasible equilibria. For disease‐selective predation model there is a high risk of prey extinction. On the other hand, for non‐disease selective predation both populations co‐exist. Local stability analysis and global stability analysis of the positive interior equilibrium are performed. Moreover, conditions for the permanence of the system are obtained. Finally, we conclude that strictly disease‐selective predation may not be acceptable for the persistence of the prey population. Copyright © 2005 John Wiley & Sons, Ltd.     

Global properties of a class of HIV infection models with Beddington–DeAngelis functional response

In this paper, the global properties of a class of human immunodeficiency virus (HIV) models with Beddington–DeAngelis functional response are investigated. Lyapunov functions are constructed to establish the global asymptotic stability of the uninfected and infected steady states of three HIV infection models. The first model considers the interaction process of the HIV and the CD4 ⁺ T cells and takes into account the latently and actively infected cells. The second model describes two co‐circulation populations of target cells, representing CD4 ⁺ T cells and macrophages. The third model is a two‐target‐cell model taking into account the latently and actively infected cells. We have proven that if the basic reproduction number R₀ is less than unity, then the uninfected steady state is globally asymptotically stable, and if R₀ > 1, then the infected steady state is globally asymptotically stable. Copyright © 2012 John Wiley & Sons, Ltd.     

Asymptotic properties of a HIV-1 infection model with time delay

Based on some important biological meanings, a class of more general HIV-1 infection models with time delay is proposed in the paper. In the HIV-1 infection model, time delay is used to describe the time between infection of uninfected target cells and the emission of viral particles on a cellular level as proposed by Herz et al. [A.V.M. Herz, S. Bonhoeffer, R.M. Anderson, R.M. May, M.A. Nowak, Viral dynamics in vivo: Limitations on estimates of intracellular delay and virus decay, Proc. Natl. Acad. Sci. USA 93 (1996) 7247-7251]. Then, the effect of time delay on stability of the equilibria of the HIV-1 infection model has been studied and sufficient criteria for local asymptotic stability of the infected equilibrium and global asymptotic stability of the viral free equilibrium are given.     

Effect of emergent carrying capacity in an eco‐epidemiological system

The paper explores an eco‐epidemiological model of a predator–prey type, where the prey population is subject to infection. The model is basically a combination of S‐I type model and a Rosenzweig–MacArthur predator–prey model. The novelty of this contribution is to consider different competition coefficients within the prey population, which leads to the emergent carrying capacity. We explicitly separate the competition between non‐infected and infected individuals. This emergent carrying capacity is markedly different to the explicit carrying capacities that have been considered in many eco‐epidemiological models. We observed that different intra‐class and inter‐class competition can facilitate the coexistence of susceptible prey‐infected prey–predator, which is impossible for the case of the explicit carrying capacity model. We also show that these findings are closely associated with bi‐stability. The present system undergoes bi‐stability in two different scenarios: (a) bi‐stability between the planner equilibria where susceptible prey co‐exists with predator or infected prey and (b) bi‐stability between co‐existence equilibrium and the planner equilibrium where susceptible prey coexists with infected prey; have been discussed. The conditions for which the system is to be permanent and the global stability of the system around disease‐free equilibrium are worked out. Copyright © 2015 John Wiley & Sons, Ltd.     

SIR DYNAMICS WITH ECONOMICALLY DRIVEN CONTACT RATES

The susceptible‐infected‐recovered (SIR) model has greatly evidenced epidemiology despite its apparent simplicity. Most applications of the SIR framework use a form of nonlinear incidence to describe the number of new cases per instant. We adapt theorems to analyze the stability of SIR models with a generalized nonlinear incidence structure. These theorems are then applied to the case of standard incidence and incidence resulting from adaptive behavioral response based on epidemiological‐economic theory. When adaptive behavior is included in the SIR model multiple equilibria and oscillatory epidemiological dynamics can occur over a greater parameter space. Our analysis, based on the epidemiological‐economic incidence, provides new insights into epidemics as complex adaptive systems, highlights important nonlinearities that lead to complex behavior, and provides mechanistic motivation for a shift away from standard incidence, and outlines important areas of research related to the complex‐adaptive dynamics of epidemics.     

Global analysis of a periodic epidemic model on cholera in presence of bacteriophage

We propose and analyze a recurrent epidemic model of cholera in the presence of bacteriophage. The model is extended by general periodic incidence functions for low‐infectious bacterium and high‐infectious bacterium, respectively. A general periodic shedding function for two infected class (phage‐positive and phage‐negative) and a generalized contact and intrinsic growth function for susceptible class are also considered. Under certain biological assumptions, we derive the basic reproduction number (R₀) in a periodic environment for the proposed model. We also observe the global stability of the disease‐free equilibrium, existence, permanence, and global stability of the positive endemic periodic solution of our proposed model. Finally, we verify our results with specific functional form. Copyright © 2016 John Wiley & Sons, Ltd.     

Stability and bifurcation in epidemic models describing the transmission of toxoplasmosis in human and cat populations

A five‐dimensional ordinary differential equation model describing the transmission of Toxoplamosis gondii disease between human and cat populations is studied in this paper. Self‐diffusion modeling the spatial dynamics of the T. gondii disease is incorporated in the ordinary differential equation model. The normalized version of both models where the unknown functions are the proportions of the susceptible, infected, and controlled individuals in the total population are analyzed. The main results presented herein are that the ODE model undergoes a trans‐critical bifurcation, the system has no periodic orbits inside the positive octant, and the endemic equilibrium is globally asymptotically stable when we restrict the model to inside of the first octant. Furthermore, a local linear stability analysis for the spatially homogeneous equilibrium points of the reaction diffusion model is carried out, and the global stability of both the disease‐free and endemic equilibria are established for the reaction–diffusion system when restricted to inside of the first octant. Finally, numerical simulations are provided to support our theoretical results and to predict some scenarios about the spread of the disease. Copyright © 2017 John Wiley & Sons, Ltd.     

Dynamical behaviors of a discrete HIV‐1 virus model with bilinear infective rate

We establish a discrete virus dynamic model by discretizing a continuous HIV‐1 virus model with bilinear infective rate using ‘hybrid’ Euler method. We discuss not only the existence and global stability of the uninfected equilibrium but also the existence and local stability of the infected equilibrium. We prove that there exists a crucial value similar to that of the continuous HIV‐1 virus dynamics, which is called the basic reproductive ratio of the virus. If the basic reproductive ratio of the virus is less than one, the uninfected equilibrium is globally asymptotically stable. If the basic reproductive ratio of the virus is larger than one, the infected equilibrium exists and is locally stable. Moreover, we consider the permanence for such a system by constructing a Lyapunov function v_n. Copyright © 2013 John Wiley & Sons, Ltd.     

Stability preserving NSFD scheme for a multi‐group SVIR epidemic model

A discrete multi‐group SVIR epidemic model with general nonlinear incidence rate and vaccination is investigated by utilizing Mickens' nonstandard finite difference scheme to a corresponding continuous model. Mathematical analysis shows that the global asymptotic stability of the equilibria is fully determined by the basic reproduction number by constructing Lyapunov functions. The results imply that the discretization scheme can efficiently preserves the global asymptotic stability of the equilibria for corresponding continuous model, and numerical simulations are carried out to illustrate the theoretical results. Copyright © 2017 John Wiley & Sons, Ltd.     

A ratio‐dependent eco‐epidemiological model of the Salton Sea

Ratio‐dependent models set up a challenging issue for their rich dynamics incomparison to prey‐dependent models. Little attention has been paid so far to describe the importance of transmissible disease in ecological situation by considering ratio‐dependent models. In this paper, by assuming the predator response function as ratio‐dependent, we consider a model of a system of three non‐linear differential equations describing the time evolution of susceptible and infected Tilapia fish population and their predator, the Pelican. Existence and stability analysis of different equilibria of the system lead to different realistic thresholds in terms of system parameters. The condition for extinction of the species is also worked out. Our analytical and numerical studies may be helpful to chalk out suitable control strategies for minimizing the extinction of the Pelicans. We also suggest that supply of alternative food source for predator population may be used as a possible solution to save the predator from their extinction. Copyright © 2005 John Wiley & Sons, Ltd.     

Stability of HIV/HTLV-I co-infection model with delays

In this paper, we formulate a within-host dynamics model for HIV/HTLV-I co-infection under the influence of cytotoxic T lymphocytes (CTLs). The model incorporates silent HIV-infected CD4⁺T cells and silent HTLV-infected CD4⁺T cells. The model includes two routes of HIV transmission, virus to cell (VTC) and cell to cell (CTC). It also incorporates two modes of HTLV-I transmission, horizontal transmission via direct CTC contact and vertical transmission through mitotic division of Tax-expressing HTLV-infected cells. The model takes into account five types of distributed-time delays. We analyze the model by proving the nonnegativity and boundedness of the solutions, calculating all possible equilibria, deriving a set of key threshold parameters, and proving the global stability of all equilibria. The global asymptotic stability of all equilibria is established by utilizing Lyapunov function and LaSalle's invariance principle. We present numerical simulations to justify the applicability and effectiveness of the theoretical results. In addition, we discuss the effect of HTLV-I infection on the HIV dynamics and vice versa.     

A fractional order HIV/AIDS model based on the effect of screening of unaware infectives

In this paper, a fractional order model for the spread of human immunodeficiency virus (HIV) infection is proposed to study the effect of screening of unaware infected individuals on the spread of the HIV virus. For this purpose, local asymptotic stability analysis of the disease‐free equilibrium is investigated. In addition, the model is studied for different values of the fractional order to show the relation between the variations of the reproduction number and the order of the proposed model. Finally, numerical solutions are simulated by using a predictor‐corrector method to illustrate the dynamics between susceptible individuals and unaware infected individuals.     

Within‐host and synaptic transmissions: contributions to the spread of HIV infection

We study the contributions of within‐host (virus‐to‐cell) and synaptic (cell‐to‐cell) transmissions in a mathematical model for human immunodeficiency virus epidemics. The model also includes drug resistance. We prove the local and global stability of the disease‐free equilibrium and the local stability of the endemic equilibrium. We analyse the effect of the cell‐to‐cell transmission rate on the value of the reproduction number, R₀. Moreover, we show evidence of a qualitative change in the models' dynamics, subjected to the value of the drug efficacy. In the end, important inferences are drawn. Copyright © 2016 John Wiley & Sons, Ltd.