GLOBAL STABILITY OF AN HIV/AIDS MODEL WITH STOCHASTIC PERTURBATION

2011 ◽  
Vol 04 (02) ◽  
pp. 349-358 ◽  
Author(s):  
Junyuan Yang ◽  
Xiaoyan Wang ◽  
Xuezhi Li

In this paper, we investigate the dynamic behavior of an HIV model with stochastic perturbation. Firstly, in ODE model, the disease-free equilibrium E0 is globally asymptotically stable if the basic reproductive number R0 < 1. When R0 > 1, the endemic equilibrium E* is globally asymptotically stable. Secondly, the criterion for robustness of the system is established under stochastic perturbations. The conditions of stochastic stability of the endemic equilibrium E* are obtained. Finally, we simulate our analytical results.

2014 ◽  
Vol 2014 ◽  
pp. 1-9
Author(s):  
Zizi Wang ◽  
Zhiming Guo

A new epidemiological model is introduced with nonlinear incidence, in which the infected disease may lose infectiousness and then evolves to a chronic noninfectious disease when the infected disease has not been cured for a certain timeτ. The existence, uniqueness, and stability of the disease-free equilibrium and endemic equilibrium are discussed. The basic reproductive numberR0is given. The model is studied in two cases: with and without time delay. For the model without time delay, the disease-free equilibrium is globally asymptotically stable provided thatR0≤1; ifR0>1, then there exists a unique endemic equilibrium, and it is globally asymptotically stable. For the model with time delay, a sufficient condition is given to ensure that the disease-free equilibrium is locally asymptotically stable. Hopf bifurcation in endemic equilibrium with respect to the timeτis also addressed.


2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Hui Zhang ◽  
Li Yingqi ◽  
Wenxiong Xu

We present an SEIS epidemic model with infective force in both latent period and infected period, which has different general saturation incidence rates. It is shown that the global dynamics are completely determined by the basic reproductive number R0. If R0≤1, the disease-free equilibrium is globally asymptotically stable in T by LaSalle’s Invariance Principle, and the disease dies out. Moreover, using the method of autonomous convergence theorem, we obtain that the unique epidemic equilibrium is globally asymptotically stable in T0, and the disease spreads to be endemic.


2017 ◽  
Vol 82 (5) ◽  
pp. 945-970 ◽  
Author(s):  
Jinliang Wang ◽  
Min Guo ◽  
Shengqiang Liu

Abstract An SVIR epidemic model with continuous age structure in the susceptibility, vaccination effects and relapse is proposed. The asymptotic smoothness, existence of a global attractor, the stability of equilibria and persistence are addressed. It is shown that if the basic reproductive number $\Re_0&lt;1$, then the disease-free equilibrium is globally asymptotically stable. If $\Re_0&gt;1$, the disease is uniformly persistent, and a Lyapunov functional is used to show that the unique endemic equilibrium is globally asymptotically stable. Combined effects of susceptibility age, vaccination age and relapse age on the basic reproductive number are discussed.


2014 ◽  
Vol 07 (05) ◽  
pp. 1450054 ◽  
Author(s):  
S. Athithan ◽  
Mini Ghosh

This paper presents a nonlinear sex-structured mathematical model to study the spread of HIV/AIDS by considering transmission of disease by heterosexual contact. The epidemic threshold and equilibria for the model are determined, local stability and global stability of both the "Disease-Free Equilibrium" (DFE) and "Endemic Equilibrium" (EE) are discussed in detail. The DFE is shown to be locally and globally stable when the basic reproductive number ℛ0 is less than unity. We also prove that the EE is locally and globally asymptotically stable under some conditions. Finally, numerical simulations are reported to support the analytical findings.


2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Qianqian Li ◽  
Shengshan Cao ◽  
Xiao Chen ◽  
Guiquan Sun ◽  
Yunxi Liu ◽  
...  

A mathematical model of HIV/AIDS transmission incorporating treatment and drug resistance was built in this study. We firstly calculated the threshold value of the basic reproductive number (R0) by the next generation matrix and then analyzed stability of two equilibriums by constructing Lyapunov function. WhenR0<1, the system was globally asymptotically stable and converged to the disease-free equilibrium. Otherwise, the system had a unique endemic equilibrium which was also globally asymptotically stable. While an antiretroviral drug tried to reduce the infection rate and prolong the patients’ survival, drug resistance was neutralizing the effects of treatment in fact.


2017 ◽  
Vol 2017 ◽  
pp. 1-12
Author(s):  
Enrique Lozano-Ochoa ◽  
Jorge Fernando Camacho ◽  
Cruz Vargas-De-León

We study an epidemiological mathematical model formulated in terms of an ODE system taking into account both social and nonsocial contagion risks of obesity. Analyzing first the case in which the model presents only the effect due to social contagion and using qualitative methods of the stability analysis, we prove that such system has at the most three equilibrium points, one disease-free equilibrium and two endemic equilibria, and also that it has no periodic orbits. Particularly, we found that when considering R0 (the basic reproductive number) as a parameter, the system exhibits a backward bifurcation: the disease-free equilibrium is stable when R0<1 and unstable when R0>1, whereas the two endemic equilibria appear from R0⁎ (a specific positive value reached by R0 and less than unity), one being asymptotically stable and the other unstable, but for R0>1 values, only the former remains inside the feasible region. On the other hand, considering social and nonsocial contagion and following the same methodology, we found that the dynamic of the model is simpler than that described above: it has a unique endemic equilibrium point that is globally asymptotically stable.


2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Jorge Fernando Camacho ◽  
Cruz Vargas-De-León

In this paper, we study a modified SIRI model without vital dynamics, based on a system of nonlinear ordinary differential equations, for epidemics that exhibit partial immunity after infection, reinfection, and disease-induced death. This model can be applied to study epidemics caused by SARS-CoV, MERS-CoV, and SARS-CoV-2 coronaviruses, since there is the possibility that, in diseases caused by these pathogens, individuals recovered from the infection have a decrease in their immunity and can be reinfected. On the other hand, it is known that, in populations infected by these coronaviruses, individuals with comorbidities or older people have significant mortality rates or deaths induced by the disease. By means of qualitative methods, we prove that such system has an endemic equilibrium and an infinite line of nonhyperbolic disease-free equilibria, we determine the local and global stability of these equilibria, and we also show that it has no periodic orbits. Furthermore, we calculate the basic reproductive number R 0 and find that the system exhibits a forward bifurcation: disease-free equilibria are stable when R 0 < 1 / σ and unstable when R 0 > 1 / σ , while the endemic equilibrium consist of an asymptotically stable upper branch that appears from R 0 > 1 / σ , σ being the rate that quantifies reinfection. We also show that this system has two conserved quantities. Additionally, we show some of the most representative numerical solutions of this system.


2020 ◽  
Vol 13 (3) ◽  
pp. 549-566
Author(s):  
Abba Mahamane Oumarou ◽  
Saley Bisso

This paper focuses on the dynamics of spreads of a coronavirus disease (Covid-19).Through this paper, we study the impact of a contact rate in the transmission of the disease. We determine the basic reproductive number R0, by using the next generation matrix method. We also determine the Disease Free Equilibrium and Endemic Equilibrium points of our model. We prove that the Disease Free Equilibrium is asymptotically stable if R0 < 1 and unstable if R0 > 1. The asymptotical stability of Endemic Equilibrium is also establish. Numerical simulations are made to show the impact of contact rate in the spread of disease.


Author(s):  
Laid Chahrazed

In this work, we consider a nonlinear epidemic model with temporary immunity and saturated incidence rate. Size N(t) at time t, is divided into three sub classes, with N(t)=S(t)+I(t)+Q(t); where S(t), I(t) and Q(t) denote the sizes of the population susceptible to disease, infectious and quarantine members with the possibility of infection through temporary immunity, respectively. We have made the following contributions: The local stabilities of the infection-free equilibrium and endemic equilibrium are; analyzed, respectively. The stability of a disease-free equilibrium and the existence of other nontrivial equilibria can be determine by the ratio called the basic reproductive number, This paper study the reduce model with replace S with N, which does not have non-trivial periodic orbits with conditions. The endemic -disease point is globally asymptotically stable if R0 ˃1; and study some proprieties of equilibrium with theorems under some conditions. Finally the stochastic stabilities with the proof of some theorems. In this work, we have used the different references cited in different studies and especially the writing of the non-linear epidemic mathematical model with [1-7]. We have used the other references for the study the different stability and other sections with [8-26]; and sometimes the previous references.


2017 ◽  
Vol 10 (02) ◽  
pp. 1750030 ◽  
Author(s):  
Shaoli Wang ◽  
Xinyu Song

Based on a multi-scale view, in this paper, we study an age-structured within-host model with Crowley–Martin functional response for the control of viral infections. By means of semigroup and Lyapunov function, the global asymptotical property of infected steady state of the model is obtained. The results show that when the basic reproductive number falls below unity, the infection dies out. However, when the basic reproductive number exceeds unity, there exists a unique positive equilibrium which is globally asymptotically stable. This model can be deduced to different viral models with or without time delay.


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