A nonlinear HIV/AIDS model with contact tracing

A nonlinear mathematical model is proposed and analyzed to study the effect of contact tracing on reducing the spread of HIV/AIDS in a homogeneous population with constant immigration of susceptibles. In modeling the dynamics, the population is divided into four subclasses of HIV negatives but susceptibles, HIV positives or infectives that do not know they are infected, HIV positives that know they are infected and that of AIDS patients. Susceptibles are assumed to become infected via sexual contacts with (both types of) infectives and all infectives move with constant rates to develop AIDS. The model is analyzed using the stability theory of differential equations and numerical simulation. The model analysis shows that contact tracing may be of immense help in reducing the spread of AIDS epidemic in a population. It is also found that the endemicity of infection is reduced when infectives after becoming aware of their infection do not take part in sexual interaction.     

Impact of optimal control on the treatment of HIV/AIDS and screening of unaware infectives

In this paper, we study the impact of optimal control on the treatment of HIV/AIDS and screening of unaware infectives on the transmission dynamics of the disease in a homogeneous population with constant immigration of susceptibles incorporating use of condom, screening of unaware infectives and treatment of the infected. Initially we consider constant controls and thereafter treat control measures as time dependent control parameters. In the constant controls case, we calculate the basic reproduction number and investigate the existence and stability of equilibria. The model is found to exhibit transcritical bifurcation. For the time dependent controls, we formulate the appropriate optimal control problem and investigate the necessary conditions for the disease control in order to determine the role of unaware infectives in the spread of HIV/AIDS. We observed that unawareness by infectives has a great cost impact on the community. We further investigate the impact of combinations of the strategies in the control of HIV/AIDS. Carrying out cost-effectiveness analysis, we found that the most cost-effective strategy is the combination of all the control strategies.     

Modelling and analysis of the spread of AIDS epidemic with immigration of HIV infectives

We propose and analyze, a nonlinear mathematical model of the spread of HIV/AIDS in a population of varying size with immigration of infectives. It is assumed that susceptibles become infected via sexual contacts with infectives (also assumed to be infectious) and all infectives ultimately develop AIDS. The model is studied using stability theory of differential equations and computer simulation. Model dynamics is also discussed under two particular cases when there is no direct inflow of infectives. On analyzing these situations, it is found that the disease is always persistent if the direct immigration of infectives is allowed in the community. Further, in the absence of inflow of infectives, the endemicity of the disease is found to be higher if pre-AIDS individuals also interact sexually in comparison to the case when they do not take part in sexual interactions. Thus, if the direct immigration of infectives is restricted, the spread of infection can be slowed down. A numerical study of the model is also carried out to investigate the influence of certain key parameters on the spread of the disease.     

Modelling the effect of tuberculosis on the spread of HIV infection in a population with density-dependent birth and death rate

A nonlinear mathematical model is proposed to study the effect of tuberculosis on the spread of HIV infection in a logistically growing human population. The host population is divided into four sub classes of susceptibles, TB infectives, HIV infectives (with or without TB) and that of AIDS patients. The model exhibits four equilibria namely, a disease free, HIV free, TB free and an endemic equilibrium. The model has been studied qualitatively using stability theory of nonlinear differential equations and computer simulation. We have found a threshold parameter R₀ which is if less than one, the disease free equilibrium is locally asymptotically stable otherwise for R₀>1, at least one of the infections will be present in the population. It is shown that the positive endemic equilibrium is always locally stable but it may become globally stable under certain conditions showing that the disease becomes endemic. It is found that as the number of TB infectives decreases due to recovery, the number of HIV infectives also decreases and endemic equilibrium tends to TB free equilibrium. It is also observed that number of AIDS individuals decreases if TB is not associated with HIV infection. A numerical study of the model is also performed to investigate the influence of certain key parameters on the spread of the disease.     

A linked risk group model for investigating the spread of HIV

This paper describes a model that simulates the spread of HIV and progression to AIDS. The model is based on classical models of disease transmission. It consists of six linked risk groups and tracks the numbers of infectives, AIDS cases, AIDS related deaths, and other deaths of infected persons in each risk group. Parametric functions are used to represent risk-group-specific and time-dependent average contact rates. Contacts are needle sharing, sexual contacts, or blood product transfers.

An important feature of the model is that the contact rate parameters are estimated by minimizing differences between AIDS incidence and reported AIDS cases adjusted for undercounting biases. This feature results in an HIV epidemic curve that is analogous to one estimated by backcalculation models but whose dynamics are determined by simulating disease transmission. The model exhibits characteristics of both the disease transmission and the backcalculation approaches, i.e., the model:

• reconstructs the historical behavior patterns of the different risk groups,

• includes separate effects of treatment and changes in average contact rates,

• accounts for other mortality risks for persons infected with HIV,

• calculates short-term projections of AIDS incidence, HIV incidence, and HIV prevalence,

• calculates cumulative HIV infections (the quantity calculated by backcalculation approaches) and HIV prevalence (the quantity measured by seroprevalence and sentinel surveys). This latter feature permits the validation of the estimates generated by two distinct approaches.

We demonstrate the use of the model with an application to U.S. AIDS data through 1991.     

Asymptotic properties of an HIV/AIDS model with a time delay

A mathematical model for HIV/AIDS with explicit incubation period is presented as a system of discrete time delay differential equations and its important mathematical features are analysed. The disease-free and endemic equilibria are found and their local stability investigated. We use the Lyapunov functional approach to show the global stability of the endemic equilibrium. Qualitative analysis of the model including positivity and boundedness of solutions, and persistence are also presented. The HIV/AIDS model is numerically analysed to asses the effects of incubation period on the dynamics of HIV/AIDS and the demographic impact of the epidemic using the demographic and epidemiological parameters for Zimbabwe.     

Modelling circumcision and condom use as HIV/AIDS preventive control strategies

We present a sex-structured model for heterosexual transmission of HIV/AIDS with explicit incubation period for modelling the effect of male circumcision as a preventive strategy for HIV/AIDS. The model is formulated using integro-differential equations, which are shown to be equivalent to delay differential equations with delay due to incubation period. The threshold and equilibria for the model are determined and stabilities are examined. We extend the model to incorporate the effects of condom use as another preventive strategy for controlling HIV/AIDS. Basic reproductive numbers for these models are computed and compared to assess the effectiveness of male circumcision and condom use in a community. The models are numerically analysed to assess the effects of the two preventive strategies on the transmission dynamics of HIV/AIDS. We conclude from the study that in the continuing absence of a preventive vaccine or cure for HIV/AIDS, male circumcision is a potential effective preventive strategy of HIV/AIDS to help communities slow the development of the HIV/AIDS epidemic and that it is even more effective if implemented jointly with condom use. The study provides insights into the possible community benefits that male circumcision and condom use as preventive strategies provide in slowing or curtailing the HIV/AIDS epidemic.     

Analysis of the dynamics of a delayed HIV pathogenesis model

In this paper, considering full Logistic proliferation of CD4⁺ T cells, we study an HIV pathogenesis model with antiretroviral therapy and HIV replication time. We first analyze the existence and stability of the equilibrium, and then investigate the effect of the time delay on the stability of the infected steady state. Sufficient conditions are given to ensure that the infected steady state is asymptotically stable for all delay. Furthermore, we apply the Nyquist criterion to estimate the length of delay for which stability continues to hold, and investigate the existence of Hopf bifurcation by using a delay τ as a bifurcation parameter. Finally, numerical simulations are presented to illustrate the main results.     

Dynamical behavior of a delay virus dynamics model with CTL immune response

In this paper, the dynamical behavior of a virus dynamics model with CTL immune response and time delay is studied. Time delay is used to describe the time between the infected cell and the emission of viral particles on a cellular level. The effect of time delay on stability of the equilibria of the CTL immune response model has been studied and sufficient criteria for local asymptotic stability of the disease-free equilibrium, immune-free equilibrium and endemic equilibrium and global asymptotic stability of the disease-free equilibrium are given. Some conditions for Hopf bifurcation around immune-free equilibrium and endemic equilibrium to occur are also obtained by using the time delay as a bifurcation parameter. Numerical simulation with some hypothetical sets of data has been done to support the analytical findings.     

Dynamics of a Predator-prey Model with Delay and Fear Effect

Recent manipulations on vertebrates showed that the fear of preda- tors, caused by prey after they perceived predation risk, could reduce the prey''s reproduction greatly. And it''s known that predator-prey systems with fear ef- fect exhibit very rich dynamics. On the other hand, incorporating the time delay into predator-prey models could also induce instability and oscillations via Hopf bifurcation. In this paper, we are interested in studying the com- bined effects of the fear effect and time delay on the dynamics of the classic Lotka-Volterra predator-prey model. It''s shown that the time delay can cause the stable equilibrium to become unstable, while the fear effect has a stabi- lizing effect on the equilibrium. In particular, the model loses stability when the delay varies and then regains its stability when the fear effect is stronger. At last, by using the normal form theory and center manifold argument, we derive explicit formulas which determine the stability and direction of periodic solutions bifurcating from Hopf bifurcation. Numerical simulations are carried to explain the mathematical conclusions.     

一类带有非线性传染率的SEIR传染病模型的全局分析

通过假设被传染的易感者一部分经过一段潜伏期后才具有传染性,而另一部分被感染的易感者直接成为传染者,建立了一类带有非线性传染率的SEIR传染病模型,得到了确定疾病是否成为地方病的基本再生数以及无病平衡点和地方病平衡点的全局稳定性.     

Stability analysis of an HIV/AIDS epidemic model with treatment

An HIV/AIDS epidemic model with treatment is investigated. The model allows for some infected individuals to move from the symptomatic phase to the asymptomatic phase by all sorts of treatment methods. We first establish the ODE treatment model with two infective stages. Mathematical analyses establish that the global dynamics of the spread of the HIV infectious disease are completely determined by the basic reproduction number _ℜ0${\Re }_0$. If _ℜ0≤1${\Re }_0\le 1$, the disease-free equilibrium is globally stable, whereas the unique infected equilibrium is globally asymptotically stable if _ℜ0>1${\Re }_0>1$. Then, we introduce a discrete time delay to the model to describe the time from the start of treatment in the symptomatic stage until treatment effects become visible. The effect of the time delay on the stability of the endemically infected equilibrium is investigated. Moreover, the delay model exhibits Hopf bifurcations by using the delay as a bifurcation parameter. Finally, numerical simulations are presented to illustrate the results.     

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.     

A delay differential equation model of HIV infection of CD4+ T-cells with cure rate

A delay differential equation as a mathematical model that described HIV infection of CD4⁺ T-cells is analyzed. When the constant death rate of infected but not yet virus-producing cells is equal to zero, the stability of the non-negative equilibria and the existence of Hopf bifurcation are investigated. A stability switch in the system due to variation of delay parameter has been observed, so is the phenomena of Hopf bifurcation and stable limit cycle. The estimation of the length of delay to preserve stability has been calculated. Further, when the constant death rate of infected but not yet virus-producing cells is not equal to zero, by using the geometric stability switch criterion in the delay differential system with delay dependent parameters, we present that stable equilibria become unstable as the time delay increases. Numerical simulations are carried out to explain the mathematical conclusions.     

Analysis of periodic solutions in an eco-epidemiological model with saturation incidence and latency delay

In the present work, a mathematical model of predator–prey ecological interaction with infected prey is investigated. A saturation incidence function is used to model the behavioral change of the susceptible individuals when their number increases or due to the crowding effect of the infected individuals [V. Capasso, G. Serio, A generalization of the Kermack–McKendrick deterministic epidemic model, Math. Biosci. 42 (1978) 41–61]. Stability criteria for the infection-free and the endemic equilibria are deduced in terms of system parameters. The basic model is then modified to incorporate a time delay, describing a latency period. Stability and bifurcation analysis of the resulting delay differential equation model is carried out and ranges of the delay inducing stability and as well as instability for the system are found. Finally, a stability analysis of the bifurcating solutions is performed and the criteria for subcritical and supercritical Hopf bifurcation derived. The existence of a delay interval that preserves the stability of periodic orbits is demonstrated. The analysis emphasizes the importance of differential predation and a latency period in controlling disease dynamics.     

Global results for an HIV/AIDS model with multiple susceptible classes and nonlinear incidence

In this paper, an HIV/AIDS epidemic model is proposed in which there are two susceptible classes. Two types of general nonlinear incidence functions are employed to depict the scenarios of infection among cautious and incautious individuals. Qualitative analyses are performed, in terms of the basic reproduction number $\R_0$, to gain the global dynamics of the model: the disease-free equilibrium is of global asymptotic stability when $\R_0\leq 1$; a unique endemic equilibrium exists and globally asymptotically stable $\R_0> 1$. The introduction of cautious susceptible and the resulting multiple transmission functions has positive effect on HIV/AIDS prevalence. Numerical simulations are carried out to illustrate and extend the obtained analytical results.     

Deriving the HIV incubation period distribution for AIDS using immunological markers and devising infection treatment strategies

Survey data suggest that it is impossible for HIV infecteds to develop AIDs if the values of their CD4+ T-cell densities are above a critical threshold. An infected whose CD4+ T-cell density falls below 200 cells per microliter is now automatically regarded as having AIDS by the CDC. Using the CD4+ T-cell density as a surrogate marker of disease progression, a model that is consistent with the data is developed and applied to the homosexual/bisexual and IVDU risk groups. Assuming that the critical CD4+ T-cell density for these risk groups are identical, it is found that their progression towards AIDS during the incubation period is identical, suggesting that the dynamics of the HIV infection may be independent of risk group. The different incubation period distributions obtained from this modelling for these two risk groups is shown to be entirely due to their different normal seronegative CD4+ T-cell density distributions. Using IFN-γ as a surrogate marker is shown to give similar results.The impact of the HIV infection on the immune system is reviewed, and immunological infection models are developed. The data suggest to this author that Homo sapiens have generally lost the ability to generate T-cells and B-cells with the specificity necessary to neutralize HIV as they evolved from the primates. It is plausible that a legacy of primate immunity to HIV still remains in the 10% of Homo sapiens who show no immune system deterioration in the first 10 years of the HIV infection. New HIV infection treatment strategies based on this model are devised and discussed.     

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.     

Study on a HIV/AIDS model with application to Yunnan province,China

This paper presents an epidemic model aiming at the prevalence of HIV/AIDS in Yunnan, China. The total population in the model is restricted within high risk population. By the epidemic characteristics of HIV/AIDS in Yunnan province, the population is divided into two groups: injecting drug users (IDUs) and people engaged in commercial sex (PECS) which includes female sex workers (FSWs), and clients of female sex workers (C). For a better understanding of HIV/AIDS transmission dynamics, we do some necessary mathematical analysis. The conditions and thresholds for the existence of four equilibria are established. We compute the reproduction number for each group independently, and show that when both the reproduction numbers are less than unity, the disease-free equilibrium is globally stable. The local stabilities for other equilibria including two boundary equilibria and one positive equilibrium are figured out. When we omit the infectivity of AIDS patients, global stability of these equilibria are obtained. For the simulation, parameters are chosen to fit as much as possible prevalence data publicly available for Yunnan. Increasing strength of the control measure on high risk population is necessary to reduce the HIV/AIDS in Yunnan.