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This study directs the discussion of HIV disease with a novel kind of complex dynamical generalized and piecewise operator in the sense of classical and Atangana Baleanu (AB) derivatives having arbitrary order. The HIV infection model has a susceptible class, a recovered class, along with a case of infection divided into three sub-different levels or categories and the recovered class. The total time interval is converted into two, which are further investigated for ordinary and fractional order operators of the AB derivative, respectively. The proposed model is tested separately for unique solutions and existence on bi intervals. The numerical solution of the proposed model is treated by the piece-wise numerical iterative scheme of Newtons Polynomial. The proposed method is established for piece-wise derivatives under natural order and non-singular Mittag-Leffler Law. The cross-over or bending characteristics in the dynamical system of HIV are easily examined by the aspect of this research having a memory effect for controlling the said disease. This study uses the neural network (NN) technique to obtain a better set of weights with low residual errors, and the epochs number is considered 1000. The obtained figures represent the approximate solution and absolute error which are tested with NN to train the data accurately. [ABSTRACT FROM AUTHOR]

Cell-to-cell infection cannot be ignored in the development of HIV in the host. The mathematical difficulty in (Wang et al. in J. Biol. Dyn. 11:455–483, 2016) is mainly due to the assumption of the equality of two parameters, in which they are the proportions of infection that lead to latency caused by virus-to-cell infection and cell-to-cell transmission, respectively. To overcome the restricted condition, we propose a more general HIV development model with virus-to-cell and cell-to-cell infection patterns with logistic growth and saturation incidence. By constructing a proper Lyapunov function we obtain the global stability of the disease-free equilibrium without this restricted condition, thereby the main result in (Wang et al. in J. Biol. Dyn. 11:455–483, 2016) removing the restricted condition is proved by using our method even if two parameters are not equal. We also investigate the existence of Hopf bifurcation of diseased equilibrium in four cases. [ABSTRACT FROM AUTHOR]

This work focuses on an HIV infection model with intracellular delay and immune response delay, in which the former delay refers to the time it takes for healthy cells to become infectious after infection, and the latter delay refers to the time when immune cells are activated and induced by infected cells. By investigating the properties of the associated characteristic equation, we derive sufficient criteria for the asymptotic stability of the equilibria and the existence of Hopf bifurcation to the delayed model. Based on normal form theory and center manifold theorem, the stability and the direction of the Hopf bifurcating periodic solutions are studied. The results reveal that the intracellular delay cannot affect the stability of the immunity-present equilibrium, but the immune response delay can destabilize the stable immunity-present equilibrium through the Hopf bifurcation. Numerical simulations are provided to support the theoretical results.

This paper aims to the investigation of the global threshold dynamics of an infection age-space structured HIV infection model. The model is formulated in a bounded domain involving two infection routes (virus-to-cell and cell-to-cell) and Neumann boundary conditions. We first transform the original model to a hybrid system containing two partial differential equations and a Volterra integral equation. By appealing to the theory of fixed point problem together with Picard sequences, the well-posedness of the model is shown by verifying that the solution exists globally and the solution is ultimately bounded. Under the Neumann boundary condition, we establish the explicit expression of the basic reproduction number. By analyzing the distribution of characteristic roots of the associated characteristic equation in terms of the basic reproduction number, we achieve the local asymptotic stability of the steady states. The global asymptotic stability of the steady states is established by the technique of Lyapunov functionals, respectively. Numerical simulations are performed to validate our theoretical results. [ABSTRACT FROM AUTHOR]

In this study, a delayed HIV stochastic model with virus-to-cell infection, cell-to-cell transmission and B-cell immune response is proposed. We first transform the stochastic differential equation with distributed delay into a high-dimensional degenerate stochastic differential equation, and then theoretically analyze the dynamic behaviour of the degenerate model. The unique global solution of the model is given by rigorous analysis. By formulating suitable Lyapunov functions, the existence of the stationary Markov process is obtained if the stochastic B-cell-activated reproduction number is greater than one. We also use the law of large numbers theorem and the spectral radius analysis method to deduce that the virus can be cleared if the stochastic B-cell-inactivated reproduction number is less than one. Through uncertainty and sensitivity analysis, we obtain key parameters that determine the value of the stochastic B-cell-activated reproduction number. Numerically, we examine that low level noise can maintain the number of the virus and B-cell populations at a certain range, while high level noise is helpful for the elimination of the virus. Furthermore, the effect of the cell-to-cell infection on model behaviour, and the influence of the key parameters on the size of the stochastic B-cell-activated reproduction number are also investigated. [ABSTRACT FROM AUTHOR]

This paper is concerned with propagation dynamics in a nonlocal dispersal HIV infection model. The existence and asymptotic behavior of traveling waves with wave speeds not less than a critical speed were derived in the recent work of Wang and Ma [J. Math. Anal. Appl. 457 (2018), pp. 868–889]. However, the asymptotic behavior of the critical traveling wave and minimum wave speed were not clarified completely. In this article, we first affirm the asymptotic behavior of the critical traveling wave at negative infinity. Then we prove the non-existence of traveling waves when either the basic reproduction number \mathcal {R}_0<1 or the wave speed is less than the critical spreed and \mathcal {R}_0>1. Our result provides a complete complement for the wave propagation in the infection model. [ABSTRACT FROM AUTHOR]

The human immunodeficiency virus (HIV) mainly attacks CD4+ T cells in the host. Chronic HIV infection gradually depletes the CD4+ T cell pool, compromising the host's immunological reaction to invasive infections and ultimately leading to acquired immunodeficiency syndrome (AIDS). The goal of this study is not to provide a qualitative description of the rich dynamic characteristics of the HIV infection model of CD4+ T cells, but to produce accurate analytical solutions to the model using the modified iterative approach. In this research, a new efficient method using the new iterative method (NIM), the coupling of the standard NIM and Laplace transform, called the modified new iterative method (MNIM), has been introduced to resolve the HIV infection model as a class of system of ordinary differential equations (ODEs). A nonlinear HIV infection dynamics model is adopted as an instance to elucidate the identification process and the solution process of MNIM, only two iterations lead to ideal results. In addition, the model has also been solved using NIM and the fourth order Runge–Kutta (RK4) method. The results indicate that the solutions by MNIM match with those of RK4 method to a minimum of eight decimal places, whereas NIM solutions are not accurate enough. Numerical comparisons between the MNIM, NIM, the classical RK4 and other methods reveal that the modified technique has potential as a tool for the nonlinear systems of ODEs. [ABSTRACT FROM AUTHOR]

Abstract In this paper, a human immunodeficiency virus (HIV) infection model that includes a protease inhibitor (PI), two intracellular delays, and a general incidence function is derived from biologically natural assumptions. The global dynamical behavior of the model in terms of the basic reproduction number R 0 $\mathcal{R}_{0}$ is investigated by the methods of Lyapunov functional and limiting system. The infection-free equilibrium is globally asymptotically stable if R 0 ≤ 1 $\mathcal{R}_{0}\leq 1$ . If R 0 > 1 $\mathcal{R}_{0}>1$ , then the positive equilibrium is globally asymptotically stable. Finally, numerical simulations are performed to illustrate the main results and to analyze thre effects of time delays and the efficacy of the PI on R 0 $\mathcal{R}_{0}$ .

Recent studies have demonstrated that both virus-to-cell infection and cell-to-cell transmission play an important role in the process of HIV infection. In this paper, stochastic perturbation is introduced into HIV model with virus-to-cell infection, cell-to-cell transmission, CTL immune response and three distributed delays. The stochastic integro-delay differential equations is transformed into a degenerate stochastic differential equations. Through rigorous analysis of the model, we obtain the solution is unique, positive and global. By constructing appropriate Lyapunov functions, the existence of the stationary Markov process is derived when the critical condition is bigger than one. Furthermore, the extinction of the virus for sufficiently big noise intensity is established. Numerically, we investigate that the small noise intensity of fluctuations could help to sustain the number of virions and CTL immune response within a certain range, while the big noise intensity may be beneficial to the extinction of the virus. We also examine that the influence of random fluctuations on model dynamics may be more significant than that of the delay.

Recent researches show that virus‐to‐cell infection and cell‐to‐cell transmission are two HIV infection modes. In this paper, we propose a delayed HIV infection model including both virus‐to‐cell infection and cell‐to‐cell transmission and cytotoxic T lymphocyte immune response. The time delay describes the phenomenon between viral entry and viral production. We show the nonnegativity and boundedness of solution, obtain the steady states, and prove local asymptotic stability of the steady states. Then the optimal control problem with antiretroviral therapy and pharmacological delay is posed. We establish and analyze two types of objective functions: one is linear control and the other is quadratic control. Numerical simulations have been performed to verify the stability of steady states and show the optimal control strategies and the effects of control on cells concentration by Matlab and Lingo. [ABSTRACT FROM AUTHOR]

The activation status can dictate the fate of an HIV-infected CD4+ T cell. Infected cells with a low level of activation remain latent and do not produce virus, while cells with a higher level of activation are more productive and thus likely to transfer more virions to uninfected cells during cell-to-cell transmission. How the activation status of infected cells affects HIV dynamics under antiretroviral therapy remains unclear. We develop a new mathematical model that structures the population of infected cells continuously according to their activation status. The effectiveness of antiretroviral drugs in blocking cell-to-cell viral transmission decreases as the level of activation of infected cells increases because the more virions are transferred from infected to uninfected cells during cell-to-cell transmission, the less effectively the treatment is able to inhibit the transmission. The basic reproduction number R0 of the model is shown to determine the existence and stability of the equilibria. Using the principal spectral theory and comparison principle, we show that the infection-free equilibrium is locally and globally asymptotically stable when R0 is less than one. By constructing Lyapunov functional, we prove that the infected equilibrium is globally asymptotically stable when R0 is greater than one. Numerical investigation shows that even when treatment can completely block cell-free virus infection, virus can still persist due to cell-to-cell transmission. The random switch between infected cells with different activation levels can also contribute to the replenishment of the latent reservoir, which is considered as a major barrier to viral eradication. This study provides a new modeling framework to study the observations, such as the low viral load persistence, extremely slow decay of latently infected cells and transient viral load measurements above the detection limit, in HIV-infected patients during suppressive antiretroviral therapy. [ABSTRACT FROM AUTHOR]

In this paper, we investigate an age-structured HIV infection model with logistic growth for target cell. We rewrite the model as an abstract non-densely defined Cauchy problem and obtain the condition which guarantees the existence of the unique positive steady state. By linearizing the model at steady state and analysing the associated characteristic transcendental equations, we study the local asymptotic stability of the steady state. Furthermore, by using Hopf bifurcation theorem in Liu et al., we show that Hopf bifurcation occurs at the positive steady state when bifurcating parameter crosses some critical values. Finally, we perform some numerical simulations to illustrate our results.

In this research work, we study the Human Immunodeficiency Virus (HIV) infection on helper T cells governed by a mathematical model consisting of a system of three first-order nonlinear differential equations. The objective of the analysis is to present an approximate mathematical solution to the model that gives the count of the numbers of uninfected and infected helper T cells and the number of free virus particles present at a given instant of time. The system of nonlinear ODEs is converted into a system of nonlinear algebraic equations using spectral collocation method with three different basis functions such as Chebyshev, Legendre and Jacobi polynomials. Some factors such as the production of helper T cells and infection of these cells play a vital role in infected and uninfected cell counts. Detailed error analysis is done to compare our results with the existing methods. It is shown that the spectral collocation method is a very reliable, efficient and robust method of solution compared to many other solution procedures available in the literature. All these results are presented in the form of tables and figures. [ABSTRACT FROM AUTHOR]

In this work, a mathematical model for the human immunodeficiency virus (HIV) infection of CD4+ T-cells by using the optimal perturbation iteration method (OPIM) is analyzed. Optimization and classical perturbation techniques are combined to build the new proposed method. The iteration algorithm for systems of nonlinear differential equations for this optimal perturbation iteration technique is constructed for the first time. A test problem has been solved and some plots are given to show the reliability and efficiency of the proposed method. Obtained results exhibit the effectiveness and accuracy of the semi-analytical technique. [ABSTRACT FROM AUTHOR]

In this paper, we investigate an age-structured HIV infection model with logistic growth for target cell. We rewrite the model as an abstract non-densely defined Cauchy problem and obtain the condition which guarantees the existence of the unique positive steady state. By linearizing the model at steady state and analysing the associated characteristic transcendental equations, we study the local asymptotic stability of the steady state. Furthermore, by using Hopf bifurcation theorem in Liu et al., we show that Hopf bifurcation occurs at the positive steady state when bifurcating parameter crosses some critical values. Finally, we perform some numerical simulations to illustrate our results. [ABSTRACT FROM AUTHOR]

Abstract HIV infection persists despite long-term administration of antiretroviral therapy. The mechanisms underlying HIV persistence are not fully understood. Direct viral transmission from infected to uninfected cells (cell-to-cell transmission) may be one of them. During cell-to-cell transmission, multiple virions are delivered to an uninfected cell, making it possible that at least one virion can escape HIV drugs and establish infection. In this paper, we develop a mathematical model that includes cell-to-cell viral transmission to study HIV persistence. During cell-to-cell transmission, it is assumed that various number of virus particles are transmitted with different probabilities and antiretroviral therapy has different effectiveness in blocking their infection. We analyze the model by deriving the basic reproduction number and investigating the stability of equilibria. Sensitivity analysis and numerical simulation show that the viral load is still sensitive to the change of the treatment effectiveness in blocking cell-free virus infection. To reduce this sensitivity, we modify the model by including density-dependent infected cell death or HIV latent infection. The model results suggest that although cell-to-cell transmission may have reduced susceptibility to HIV drugs, HIV latency represents a major reason for HIV persistence in patients on suppressive treatment. [ABSTRACT FROM AUTHOR]

In this paper, we investigate the dynamical properties for a model of delayed differential equations which describes a virus–immune interaction in vivo. The model has two time delays describing time needed for infection of cell and CTLs generation. The model admits three possible equilibria: infection-free equilibrium, CTL-absent infection equilibrium and CTL-present infection equilibrium. The effect of time delay on stability of the equilibria for the CTL immune response model has been studied. [ABSTRACT FROM AUTHOR]

In this paper, the model of HIV infection of CD4+ T cells is considered as a system of fractional differential equations. Then, a numerical method by using collocation method based on the Müntz-Legendre polynomials to approximate solution of the model is presented. The application of the proposed numerical method causes fractional differential equations system to convert into the algebraic equations system. The new system can be solved by one of the existing methods. Finally, we compare the result of this numerical method with the result of the methods have already been presented in the literature.

We make a mathematical analysis of an age structured HIV infection model with both virus-to-cell and cell-to-cell transmissions to understand the dynamical behavior of HIV infection in vivo. In the model, we consider the proliferation of uninfected CD 4 + T cells by a logistic function and the infected CD 4 + T cells are assumed to have an infection-age structure. Our main results concern the Hopf bifurcation of the model by using the theory of integrated semigroup and the Hopf bifurcation theory for semilinear equations with nondense domain. Bifurcation analysis indicates that there exist some parameter values such that this HIV infection model has a nontrivial periodic solution which bifurcates from the positive equilibrium. The numerical simulations are also carried out. [ABSTRACT FROM AUTHOR]

In this work, biologically-inspired computing framework is developed for HIV infection of CD4 T-cell model using feed-forward artificial neural networks (ANNs), genetic algorithms (GAs), sequential quadratic programming (SQP) and hybrid approach based on GA-SQP. The mathematical model for HIV infection of CD4 T-cells is represented with the help of initial value problems (IVPs) based on the system of ordinary differential equations (ODEs). The ANN model for the system is constructed by exploiting its strength of universal approximation. An objective function is developed for the system through unsupervised error using ANNs in the mean square sense. Training with weights of ANNs is carried out with GAs for effective global search supported with SQP for efficient local search. The proposed scheme is evaluated on a number of scenarios for the HIV infection model by taking the different levels for infected cells, natural substitution rates of uninfected cells, and virus particles. Comparisons of the approximate solutions are made with results of Adams numerical solver to establish the correctness of the proposed scheme. Accuracy and convergence of the approach are validated through the results of statistical analysis based on the sufficient large number of independent runs. [ABSTRACT FROM AUTHOR]

In this paper, the Pseudospectral Legendre (PL) method is presented to approximate the solution of the HIV infection model of CD4+T cells. The method is based on the Lagrangian interpo- lation and the zeros of Legendre polynomial. Using the proposed method, the given system of three differential equations is converted into a system of algebraic equations. By solving the system of the algebraic equations, the unknown coefficients are computed and then the approximate solutions are obtained. The main aim of this paper is to demonstrate the PL method, and a comparison is made with the existing methods in the literature. [ABSTRACT FROM AUTHOR]

A modified mathematical model describing the human immunodeficiency virus (HIV) pathogenesis with cytotoxic T-lymphocytes (CTL) and infected cells in eclipse phase is presented and studied in this paper. The model under consideration also includes a saturated rate describing viral infection. First, the positivity and boundedness of solutions for nonnegative initial data are proved. Next, the global stability of the disease free steady state and the endemic steady states are established depending on the basic reproduction number R0 and the CTL immune response reproduction number RCTL. Moreover, numerical simulations are performed in order to show the numerical stability for each steady state and to support our theoretical findings. Our model based findings suggest that system immunity represented by CTL may control viral replication and reduce the infection. [ABSTRACT FROM AUTHOR]

In this paper, the global dynamical behaviors for a four-dimensional HIV infection model with intracellular delay and production delay which describes the interactions of cytotoxic T-lymphocyte (CTL) immune responses and general incidence rate are investigated. By using suitable Lyapunov functionals and LaSalle's invariance principle, the global stability of infection-free equilibrium, CTL-absent infection equilibrium and CTL-present infection equilibrium are established, respectively. These results can be applied to a variety of viral infection diseases that would make it possible to devise optimal treatment strategies. Numerical simulations are presented to verify the analytical results. [ABSTRACT FROM AUTHOR]

In this paper, the model of HIV infection of CD4+T cells is considered as a system of fractional differential equations. Then, a numerical method by using collocation method based on the Müntz-Legendre polynomials to approximate solution of the model is presented. The application of the proposed numerical method causes fractional differential equations system to convert into the algebraic equations system. The new system can be solved by one of the existing methods. Finally, we compare the result of this numerical method with the result of the methods have already been presented in the literature. [ABSTRACT FROM AUTHOR]

A modified mathematical model describing the human immunodeficiency virus (HIV) pathogenesis with cytotoxic T-lymphocytes (CTL) and infected cells in eclipse phase is presented and studied in this paper. The model under consideration also includes a saturated rate describing viral infection. First, the positivity and boundedness of solutions for nonnegative initial data are proved. Next, the global stability of the disease free steady state and the endemic steady states are established depending on the basic reproduction number R 0 and the CTL immune response reproduction number R C T L . Moreover, numerical simulations are performed in order to show the numerical stability for each steady state and to support our theoretical findings. Our model based findings suggest that system immunity represented by CTL may control viral replication and reduce the infection.

Fractional order derivative is nonlocal which exhibits a long time memory behavior. With advantage of these, fractional order dynamic system models are more accurate than integer order ones in understanding the dynamic behavior of bioprocesses such as HIV infection. In this paper, we systematically study the existence of positive solutions of an abstract fractional semipositone differential system involving integral boundary conditions arising from the study of HIV infection models. By using the fixed point theorem in cone, some new results are established and an example is given to demonstrate the application of our main results. [ABSTRACT FROM AUTHOR]

This work focuses on an HIV infection model with intracellular delay and immune response delay, in which the former delay refers to the time it takes for healthy cells to become infectious after infection, and the latter delay refers to the time when immune cells are activated and induced by infected cells. By investigating the properties of the associated characteristic equation, we derive sufficient criteria for the asymptotic stability of the equilibria and the existence of Hopf bifurcation to the delayed model. Based on normal form theory and center manifold theorem, the stability and the direction of the Hopf bifurcating periodic solutions are studied. The results reveal that the intracellular delay cannot affect the stability of the immunity-present equilibrium, but the immune response delay can destabilize the stable immunity-present equilibrium through the Hopf bifurcation. Numerical simulations are provided to support the theoretical results.

Abstract: In this paper, the homotopy analysis method (HAM) is investigated to give an approximate solution of a model for HIV infection of CD4+ T-cells. This method allows for the solution of the governing differential equation to be calculated in the form of an infinite series with components which can be easily calculated. The HAM utilizes a simple method to adjust and control the convergence region of the infinite series solution by using an auxiliary parameter. The results obtained are presented, and six terms are sufficient to obtain an approximation solution that is very accurate. [Copyright &y& Elsevier]

• A stochastic HIV model with cell-free and cell-to-cell infections is formulated. • The positive and global solution of the model is rigorously verified. • Existence of the unique ergodic stationary distribution of the system is studied. • Probability density function is derived by applying asymptotic analysis. • The effects of noise and cell-to-cell infection on model behavior are investigated. In this paper, a stochastic HIV model with CD 4 + T-cell proliferation, cell-free infection and cell-to-cell transmission is proposed. By constructing suitable Lyapunov function, we establish the existence of unique and ergodic stationary distribution of the model. Moreover, by using asymptotic analysis and employing the Fokker-Planck equation, we derive the probability density function around the quasi-steady state of the system. Through numerical simulations, the effects of the stochastic perturbation and cell-to-cell infection on model dynamic behavior are investigated, thus the probability density function of the system is also given under the realistic parameter values. [ABSTRACT FROM AUTHOR]

This article concerns with the infection dynamics of fractionally extended HIV infection model incorporating antibody and cytotoxic T-Lymphocyte (CTL) immune responses. We study the role of antiretroviral therapy drugs, namely, reverse transcriptase and protease inhibitors in suppressing the HIV infection. The dynamical characteristics of the system are first discussed qualitatively through linear stability of stationary states and stable regions of the infectious and infection free steady states are figured out. The obtained results are compared with the results of integer order to understand the role of fractional order derivatives in HIV infection model. Besides the qualitative analysis on the system, we also look for the solution of the fractional system through numerical simulation. [ABSTRACT FROM AUTHOR]

In this paper, a human immunodeficiency virus (HIV) infection model that includes a protease inhibitor (PI), two intracellular delays, and a general incidence function is derived from biologically natural assumptions. The global dynamical behavior of the model in terms of the basic reproduction number R 0 is investigated by the methods of Lyapunov functional and limiting system. The infection-free equilibrium is globally asymptotically stable if R 0 ≤ 1 . If R 0 > 1 , then the positive equilibrium is globally asymptotically stable. Finally, numerical simulations are performed to illustrate the main results and to analyze thre effects of time delays and the efficacy of the PI on R 0 . [ABSTRACT FROM AUTHOR]

Recent studies have demonstrated that both virus-to-cell infection and cell-to-cell transmission play an important role in the process of HIV infection. In this paper, stochastic perturbation is introduced into HIV model with virus-to-cell infection, cell-to-cell transmission, CTL immune response and three distributed delays. The stochastic integro-delay differential equations is transformed into a degenerate stochastic differential equations. Through rigorous analysis of the model, we obtain the solution is unique, positive and global. By constructing appropriate Lyapunov functions, the existence of the stationary Markov process is derived when the critical condition is bigger than one. Furthermore, the extinction of the virus for sufficiently big noise intensity is established. Numerically, we investigate that the small noise intensity of fluctuations could help to sustain the number of virions and CTL immune response within a certain range, while the big noise intensity may be beneficial to the extinction of the virus. We also examine that the influence of random fluctuations on model dynamics may be more significant than that of the delay.