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The spreading of HIV or HTLV-I among the cells has received the great attention in recent modelling study to explore the virus infection dynamics. The co-infection of HIV and HTLV-I with the effect of Cytotoxic T-lymphocytes (CTLs) immune response is also important from epidemiological point of view. To identify the co-infection scenario of HIV and HTLV-I with the CTLs effect we proposed in this paper a six compartmental ODE-model with uninfected, HIV-infected, HTLV-I infected CD4+T cells and free HIV virus particles with HIV specific CTLs and HTLV-I specific CTLs. The rates of infection of the cases are considered here saturated type and proliferation rate of uninfected and HIV infected CD4+ T-cells are of logistic terms. To establish the well-posedness of the model we have shown that the solution of the proposed model is non-negative and bounded. We obtain the basic reproduction number which is the maximum of the HIV-related reproduction and the HTLV-I related reproduction number. Along with the disease free equilibrium point the system contains other seven endemic equilibrium points containing infection by single disease or both. Analytically, we establish the local and global stability conditions of the equilibrium points and also we establish that the system experiences transcritical bifurcation by the generation of only HIV or HTLV-I infected endemic equilibrium point. Using numerical simulations, we validate the theoretical results and found two infection paths, one initiating with HIV and other with HTLV-I, both cases ultimately become co-infected. Finally, using the optimal control analysis we found the optimal policy for treatment using AVR, RTI & PI for HIV or AZT for HTLV-I control and lastly concluded by some recommendations. • A co-infected HIV & HTLV-I infection model in vivo. • Proliferation of CD4+ T-cells are taken in logistic form. • Incidence rate is taken as saturated type. • Verified competitive exclusive principle. • Spreading path has been studied using Flow-diagram. • Three types of control strategies are investigated. [ABSTRACT FROM AUTHOR]

HIV can infect different cell populations such as CD4+ T cells and macrophages. In this paper, we study the global property of the solution of an HIV model with two target cell populations. The model includes general nonlinear rates of viral infection and cell death. For each class of target cells, the time delay between viral entry into cells and viral production is included in the model. We obtain the basic reproductive number of the model, which is shown to provide a threshold condition determining the long-term behavior of the solution of the model. Specifically, we show that the infection-free equilibrium is globally asymptotically stable when the basic reproductive number is less than or equal to 1, and that the infected equilibrium is globally asymptotically stable when the basic reproductive number is greater than 1. We also extend the model with two target cell populations to a general model with n populations. Similar global properties are obtained for the general model. Numerical simulations are performed to illustrate the stability results and to evaluate the relative contribution to viral production from the two cell populations. [ABSTRACT FROM AUTHOR]

Abstract: This paper investigates a viral infection model with periodic immune response and nonlinear cytotoxic T lymphocyte (CTL) response. Using the periodic rhythms of human immune system, the model can avoid the unreasonable equilibrium in the basic viral model with nonlinear CTL response introduced by Nowak et al. We obtain the global stability of the infection-free equilibrium and the immune-exhausted equilibrium. Numerical simulations show that the oscillation of immune system can affect the pattern of the viral dynamical behaviors. Period doubling bifurcations of the system are observed via simulations. This can provide a possible interpretation for the viral oscillation behaviors, which were observed in chronic HBV and HCV infection patients. [ABSTRACT FROM AUTHOR]

This paper proposes and analyzes an adaptive immunity HIV infection model. The model describes the interaction between healthy CD 4 + T cells, silent (latent) infected cells, active infected cells, free HIV particles, Cytotoxic T lymphocytes (CTLs) and antibodies. The healthy CD 4 + T cells can be infected when they are contacted by one of the following: (i) free HIV particles, and this is known as virus-to-cell (VTC) transmission (ii) silent infected cells, and we call this mode of infection as silent HIV-infected cell-to-cell (CTC) transmission, and (iii) active infected cells, and we call this mechanism active HIV-infected CTC transmission. The incidence rates of the healthy CD 4 + T cells with free HIV particles, silent infected cells, and active infected cells are given by general functions. Moreover, the production/proliferation and removal/death rates of all compartments are represented by general functions. The model is an improvement of the existing HIV infection models which have neglected the incidence between the silent infected cells and healthy CD 4 + T cells. We first show that the model is well-posed. Then, we show that the model has five equilibria and their existence are governed by five threshold parameters. Under a set of conditions on the general functions and the threshold parameters, we have proven the global asymptotic stability of all equilibria by using Lyapunov's method. We have illustrated the theoretical results via numerical simulations. We have studied the effect of CTC transmission on the dynamical behavior of the system. We have shown that inclusion of CTC transmission decreases the concentration of the healthy CD4 + T cells and increases the concentrations of the infected cells and free HIV particles. [ABSTRACT FROM AUTHOR]