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This paper develops a mathematical model to investigate the Human Immunodeficiency Virus (HIV) infection dynamics. The model includes two transmission modes (cell-to-cell and cell-free), two adaptive immune responses (cytotoxic T-lymphocyte (CTL) and antibody), a saturated CTL immune response, and latent HIV infection. The existence and local stability of equilibria are fully characterized by four reproduction numbers. Through sensitivity analyses, we assess the partial rank correlation coefficients of these reproduction numbers and identify that the infection rate via cell-to-cell transmission, the number of new viruses produced by each infected cell during its life cycle, the clearance rate of free virions, and immune parameters have the greatest impact on the reproduction numbers. Additionally, we compare the effects of immune stimulation and cell-to-cell spread on the model's dynamics. The findings highlight the significance of adaptive immune responses in increasing the population of uninfected cells and reducing the numbers of latent cells, infected cells, and viruses. Furthermore, cell-to-cell transmission is identified as a facilitator of HIV transmission. The analytical and numerical results presented in this study contribute to a better understanding of HIV dynamics and can potentially aid in improving HIV management strategies. [ABSTRACT FROM AUTHOR]

This paper mainly targets to deduce an optimal treatment strategy for combined antiretroviral drugs, which can maximize healthy CD4+ T cells level with minimum side effects and cost. For this purpose, we consider a within-host treatment model for the HIV infection with two controls incorporating full logistic proliferation of healthy CD4+ T cells, cure rate and fusion effect. These two controls represent the effects of reverse transcriptase inhibitors (RTIs) and protease inhibitors (PIs), respectively. The model analysis begins with proving different basic properties like non-negativity, boundedness of the model solutions and calculation of the basic reproduction number of the model under consideration. Then, stability results are obtained for HIV infection-free equilibrium point and also, a critical efficacy for the combined therapies is calculated. After that, the optimal control problem is proposed and solved numerically using a forward–backward iterative method. Finally, we obtain an optimal treatment strategy that can maximize healthy CD4+ T cells count and control the viral load, and HIV-infected CD4+ T cells count to an undetectable level resulting in improved health conditions of infected individuals. [ABSTRACT FROM AUTHOR]

In this paper, we propose detailed and reasonable viral dynamics by using a multi-compartment model that incorporating the age since the infection of multiple infected cells, multiple target cells (Langerhans-cells and CD4 + T-cells), multiple viral strains (CCR5 and CXR4 HIV) and multiple infection routes (cell-to-cell and cell-to-virus). The basic reproduction number, R 0 , of the whole model is derived from two transmission mechanisms: one is the potential trigger from the infection routes for a single target cell and other is the joint effect of multiple viral infections for multi-target cells. Accordingly, we study the global stability of the steady states for the single target model. For the whole model, we prove that the infection-free steady state is globally asymptotically stable if R 0 < 1 , whereas viruses persist uniformly if R 0 > 1. Numerical simulations are carried out to illustrate the theoretical results. Sensitive analyses expound the effect of model parameters on the comprehensive reproduction number. It is remarkable to find that simultaneous control of HIV infection for two target cells can effectively reduce the viral loads within-host. Finally, our work suggests that the synergetic mechanism of multi-target cells and multi-strain cannot be ignored during treatment. [ABSTRACT FROM AUTHOR]

In this paper, a neuro-optimized numerical method is presented for approximation of HIV virus progression model in the human body. The model is composed of coupled nonlinear system of differential equations (DEs) containing healthy and infected T-Cells and HIV free virus particles. The coupled system is transformed into feedforward artificial neural network (ANN) with Mexican hat wavelet function in the hidden layers. Two meta-heuristic algorithms based on chaotic particle swarm optimization (CPSO) and its hybrid version with local search technique are exploited to tune the parameters of ANN in an unsupervised manner of error function. A comprehensive testbed is established to observe the virus growth per day with performance metric containing fitness value, computational time complexity and convergence. The proposed solutions are compared with state of art Runge–Kutta method and Legendre Wavelet Collocation Method (LWCM). The core advantages of the proposed scheme are getting the solution on continuous grid, consistent convergence, simplicity in implementation and handling strong nonlinearity effectively. [ABSTRACT FROM AUTHOR]

HIV infection is one of the most serious causes of death throughout the world. CD4+ T cells which play an important role in immune protection, are the primary targets for HIV infection. The hallmark of HIV infection is the progressive loss in population of CD4+ T cells. However, the pathway causing this slow T cell decline is poorly understood [16]. This paper studies a discontinuous mathematical model for HIV-1 infection, to investigate the effect of pyroptosis on the disease. For this purpose, we use the theory of discontinuous dynamical systems. In this way, we can better analyze the dynamical behavior of the HIV-1 system. Especially, considering the dynamics of the system on its discontinuity boundary enables us to obtain more comprehensive results rather than the previous researches. A stability region for the system, corresponding to its equilibria on the discontinuity boundary, will be determined. In such a parametric region, the trajectories of the system will be trapped on the discontinuity manifold forever. It is also shown that in the obtained stability region, the disease can lead to a steady state in which the population of uninfected T cells and viruses will preserve at a constant level of cytokines. This means that the pyroptosis will be restricted and the disease cannot progress for a long time. Some numerical simulations based on clinical and experimental data are given which are in good agreement with our theoretical results. [ABSTRACT FROM AUTHOR]

In this paper, we analyze a nonlinear mathematical model of the 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. We consider constant controls and thereafter by incorporating the theory of Volterra-Lyapunov stable matrices into the classical method of Lyapunov functions, we present an approach for global stability analysis of HIV/AIDS. The analysis and results presented in this paper make building blocks toward a comprehensive study and deeper understanding of the fundamental mechanism in HIV/AIDS. A numerical study of the model is also carried out to investigate the analytical results. [ABSTRACT FROM AUTHOR]

In this paper, a human immunodeficiency virus (HIV) infection model with both the types of immune responses, the antibody and the killer cell immune responses has been introduced. The model has been made more logical by including two delays in the activation of both the immune responses, along with the combination drug therapy. The inclusion of both the delayed immune responses provides a greater understanding of long-term dynamics of the disease. The dependence of the stability of the steady states of the model on the reproduction number R 0 has been explored through stability theory. Moreover, the global stability analysis of the infection-free steady state and the infected steady state has been proved with respect to R 0 . The bifurcation analysis of the infected steady state with respect to both delays has been performed. Numerical simulations have been carried out to justify the results proved. This model is capable of explaining the long-term dynamics of HIV infection to a greater extent than that of the existing model as it captures some basic parameters involved in the system such as immunological delay and immune response. Similarly, the model also explains the basic understanding of the disease dynamics as a result of activation of the immune response toward the virus. [ABSTRACT FROM AUTHOR]

In this paper, the human immunodeficiency virus (HIV) infection model of CDT-cells is considered. In order to numerically solve the model problem, an operational method is proposed. For that purpose, we construct the operational matrix of integration for bases of Taylor polynomials. Then, by using this matrix operation and approximation by polynomials, the HIV infection problem is transformed into a system of algebraic equations, whose roots are used to determine the approximate solutions. An important feature of the method is that it does not require collocation points. In addition, an error estimation technique is presented. We apply the present method to two numerical examples and compare our results with other methods. [ABSTRACT FROM AUTHOR]

In this paper, a fractional-order model which describes the human immunodeficiency type-1 virus (HIV-1) infection is presented. Numerical solutions are obtained using a generalized Euler method (GEM) to handle the fractional derivatives. The fractional derivatives are described in the Caputo sense. We show that the model established in this paper possesses non-negative solutions. Comparisons between the results of the fractional-order model, the results of the integer model and the measured real data obtained from 10 patients during primary HIV-1 infection are presented. These comparisons show that the results of the fractional-order model give predictions to the plasma virus load of the patients better than those of the integer model. [ABSTRACT FROM AUTHOR]

In this paper, following a previous paper ([32] Permanence and extinction of a non-autonomous HIV-1 model with two time delays, preprint) on the permanence and extinction of a delayed non-autonomous HIV-1 within-host model, we introduce and investigate a delayed HIV-1 model including maximum homeostatic proliferation rate of CD4+ T-cells and varying coefficients. By applying the asymptotic analysis theory and oscillation theory, we show: (i) the system will be permanent when the threshold value R* > 1, and for this case we also obtain the explicit estimate of the eventual lower bound of the HIV-1 virus load; (ii) the threshold value R* < 1 implies the extinction of the virus. Furthermore, we obtain that the threshold dynamics is in agreement with that of the corresponding autonomous system, which extends the classic results for the system with constant coefficients. Numerical simulations are also given to illustrate our main results, and in particular, some sensitivity test of R* is established. [ABSTRACT FROM AUTHOR]

In this paper, two delay differential systems are considered, namely, a famous model from mathematical biology about the spread of HIV viruses in blood and the advanced Lorenz system from mathematical physics. We then apply the homotopy perturbation method (HPM) to find their approximate solutions. It turns out that the method gives rise to easily obtainable solutions. In addition, residual error functions of the solutions are graphed and it is shown that increasing the parameter in the method improves the results in both cases. [ABSTRACT FROM AUTHOR]

In this paper, we revisit the model by Guedj et al. [J. Guedj, R. Thibaut and D. Commenges, Maximum likelihood estimation in dynamical models of HIV, Biometrics 63 (2007) 198-206; J. Guedj, R. Thibaut and D. Commenges, Practical identifiability of HIV dynamics models, Bull. Math. Biol. 69 (2007) 2493-2513] which describes the effect of treatment with reverse transcriptase (RT) inhibitors and incorporates the class of quiescent cells. We prove that there is a threshold value of drug efficiency such that if , the basic reproduction number and the infection is cleared and if , the infectious equilibrium is globally asymptotically stable. When the drug efficiency function is periodic and of the bang-bang type we establish a threshold, in terms of spectral radius of some matrix, between the clearance and the persistence of the disease. As stated in related works [L. Rong, Z. Feng and A. Perelson, Emergence of HIV-1 drug resistance during antiretroviral treatment, Bull. Math. Biol. 69 (2007) 2027-2060; P. De Leenheer, Within-host virus models with periodic antiviral therapy, Bull. Math. Biol. 71 (2009) 189-210.], we prove that the increase of the drug efficiency or the active duration of drug must clear the infection more quickly. We illustrate our results by some numerical simulations. [ABSTRACT FROM AUTHOR]

United Nations Political Declaration 2011 on HIV and AIDS calls to reduce the sexual transmission and the transmission of HIV among people, who inject drugs by by 2015, through different control strategies and precautionary measures. In this paper, we propose and study a simple SI type model that considers the effect of various precautionary measures to control HIV epidemic. We show, unlike conventional epidemic models, that the basic reproduction number which essentially considered as the disease eradication condition is no longer sufficient to eliminate HIV infection. In particular, we show that even when the basic reproduction number is made less than unity, the disease may persist if the initial outbreak is not low. Eradication of disease is however guaranteed if the ensemble control measure exceeds some upper critical value. It is also shown that an epidemic model with mass action incidence may exhibit backward bifurcation and bistability if density-dependent demography is considered. Our theoretical study thus indicates that extra attention should be given in controlling HIV epidemic to achieve the desired result. [ABSTRACT FROM AUTHOR]

In this paper, an exponential method is presented for the approximate solutions of the HIV infection model of CD4T. The method is based on exponential polynomials and collocation points. This model problem corresponds to a system of nonlinear ordinary differential equations. Matrix relations are constructed for the exponential functions. By aid of these matrix relations and the collocation points, the proposed technique transforms the model problem into a system of nonlinear algebraic equations. By solving the system of the algebraic equations, the unknown coefficients are computed and thus the approximate solutions are obtained. The applications of the method for the considered problem are given and the comparisons are made with the other methods. [ABSTRACT FROM AUTHOR]

Ever since HIV was first diagnosed in human, a great number of scientific works have been undertaken to explore the biological mechanisms involved in the infection and progression of the disease. This paper deals with stability and bifurcation analyses of mathematical model that represents the dynamics of HIV infection of thymus. The existence and stability of the equilibria are investigated. The model is described by a system of delay differential equations with logistic growth term, cure rate and discrete type of time delay. Choosing the time delay as a bifurcation parameter, the analysis is mainly focused on the Hopf bifurcation problem to predict the existence of a limit cycle bifurcating from the infected steady state. Further, using center manifold theory and normal form method we derive explicit formulae to determine the stability and direction of the limit cycles. Moreover the mitosis rate r also plays a vital role in the model, so we fix it as second bifurcation parameter in the incidence of viral infection. Our analysis shows that, while both the bifurcation parameters can destabilize the equilibrium E* and cause limit cycles. Numerical simulations are performed to investigate the qualitative behaviors of the inherent model. [ABSTRACT FROM AUTHOR]

A nonlinear mathematical HIV-TB model with infection-age is proposed in this paper. The basic reproduction numbers according to HIV and TB are respectively determined whether one of the diseases dies out or persists. The local and global stability of the disease-free and dominated equilibria are discussed by employing integral semigroup theory and Lyapunov functionals. The persistence of the system is also obtained by the persistence theories of the systems. The simulation illustrates the theoretical results. [ABSTRACT FROM AUTHOR]

In this paper, we investigate global dynamics for an in-host HIV-1 infection model with the long-lived infected cells and four intracellular delays. Our model admits two possible equilibria, an uninfected equilibrium and infected equilibrium depending on the basic reproduction number. We derive that the global dynamics are completely determined by the values of the basic reproduction number: if the basic reproduction number is less than one, the uninfected equilibrium is globally asymptotically stable, and the virus is cleared; if the basic reproduction number is larger than one, then the infection persists, and the infected equilibrium is globally asymptotically stable. [ABSTRACT FROM AUTHOR]