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This paper aims to analyse stability and Hopf bifurcation of the HIV-1 model with immune delay under the functional response of the Holling II type. The global stability analysis has been considered by Lyapunov–LaSalle theorem. And stability and the sufficient condition for the existence of Hopf Bifurcation of the infected equilibrium of the HIV-1 model with immune response are also studied. Some numerical simulations verify the above results. Finally, we propose a novel three dimension system to the future study. [ABSTRACT FROM AUTHOR]

In this paper, a deterministic model characterizing the within-host infection of Hepatitis C virus (HCV) in intrahepatic and extrahepatic tissues is presented. In addition, the model also includes the effect of the cytotoxic T lymphocyte (CTL) immunity described by a linear activation rate by infected cells. Firstly, the non-negativity and boundedness of solutions of the model are established. Secondly, the basic reproduction number R 01 and immune reproduction number R 02 are calculated, respectively. Three equilibria, namely, infection-free, CTL immune response-free and infected equilibrium with CTL immune response are discussed in terms of these two thresholds. Thirdly, the stability of these three equilibria is investigated theoretically as well as numerically. The results show that when R 01 < 1 , the virus will be cleared out eventually and the CTL immune response will also disappear; when R 02 < 1 < R 01 , the virus persists within the host, but the CTL immune response disappears eventually; when R 02 > 1 , both of the virus and the CTL immune response persist within the host. Finally, a brief discussion will be given. [ABSTRACT FROM AUTHOR]

This paper introduces a novel immuno-eco-epidemiological model of competition in which one of the species is affected by a pathogen. The infected individuals from species one are structured by time since- infection and the within-host dynamics of the pathogen and the immune response is also modelled. A novel feature of the model is the impact of the species two numbers on the ability of species one to mount an immune response. The within-host model has three equilibria: an extinction equilibrium, pathogen-only equilibrium and pathogen and immune response equilibrium which exists if the immune response reproduction number R0 > 1. The extinction equilibrium is always unstable, the pathogen-only equilibrium is stable if R0 < 1, and the coexistence equilibrium is stable whenever it exists. The between-host competition model has six equilibria: an extinction equilibrium, three disease-free equilibria: species one-only equilibrium, species two-only equilibrium and a disease-free species coexistence equilibrium. There are also two disease-present equilibria: species one-only disease equilibrium and disease coexistence equilibrium. The existence and stability of these equilibria are governed by six reproduction numbers. Results show that for a nonfatal disease, the disease coexistence equilibrium is stable whenever it exists. [ABSTRACT FROM AUTHOR]

In this paper, we propose and analyse a virus dynamics model with humoral immune response including latently infected cells. The incidence rate is given by Beddington–DeAngelis functional response. We have derived two threshold parameters, the basic infection reproduction numberand the humoral immune response activation numberwhich completely determined the basic and global properties of the virus dynamics model. By constructing suitable Lyapunov functions and applying LaSalle's invariance principle we have proven that if, then the infection-free equilibrium is globally asymptotically stable (GAS), if, then the chronic-infection equilibrium without humoral immune response is GAS, and if, then the chronic-infection equilibrium with humoral immune response is globally asymptotically stable. These results are further illustrated by numerical simulations. [ABSTRACT FROM PUBLISHER]

In this paper, on the basis of the simplified two-dimensional virus infection dynamics model, we propose two extended models that aim at incorporating the influence of activation-induced apoptosis which directly affects the population of uninfected cells. The theoretical analysis shows that increasing apoptosis plays a positive role in control of virus infection. However, after being included the third population of cytotoxic T lymphocytes immune response in HIV-infected patients, it shows that depending on intensity of the apoptosis of healthy cells, the apoptosis can either promote or comfort the long-term evolution of HIV infection. Further, the discrete-time delay of apoptosis is incorporated into the pervious model. Stability switching occurs as the time delay in apoptosis increases. Numerical simulations are performed to illustrate the theoretical results and display the different impacts of a delay in apoptosis. [ABSTRACT FROM AUTHOR]