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The time fractional-order nonlinear model of HIV-1 infection of T-cells with and without the rate of virus-producing cells’ death is very important in mathematical modeling. This paper presents proofs of the existence and uniqueness theorems using the Banach fixed point theorem, along with new approximate analytical solutions to two nonlinear fractional Equationuations characterizing HIV-1 infection in $CD{4^ + }$CD4+ T-cells. We use a combination of two methods, namely the natural transform method to deal with the linear terms and the Adomian decomposition method to deal with the nonlinear terms. There are two nonlinear numerical examples presented in this work, namely, we find approximate solutions to the time fractional-order nonlinear model of HIV-1 infection of T cells with and without the rate of virus-producing cells’ death using an effective method called the Adomian natural decomposition method (ANDM). The present approach, which has numerous applications in the science and engineering fields, is a great alternative to the many existing methods for solving systems of differential Equationuations. It also holds great promise for additional real-world applications. The Mathematica 12 package is used to carry out some of the nonlinear term calculations and the graphs presented in this work. [ABSTRACT FROM AUTHOR]

In this paper, we incorporate immune systems containing Cytotoxic T lymphocyte and humoral immunity into a general human immunodeficiency viruses infection model, which also considers logistic growth for target cells and both modes of spread, cell-to-cell and cell-free represents, by linear functions. We derive five threshold parameters which are used to study the existence of equilibria. By considering the characteristic equations, the local stability of disease-free and immune-free equilibria is investigated. Lyapunov functions and LaSalle's invariance are constructed to prove the global stability of all steady states. Global dynamics of the human immunodeficiency viruses model can be accurately expressed by threshold parameters; also the existence of Hopf bifurcation is discussed and the results are expressed in the form of a proposition. Furthermore, numerical simulations confirm the corresponding theoretical results. [ABSTRACT FROM AUTHOR]

In this paper, the dynamical behaviors of a multiple delayed HIV-1 infection model which describes the interactions of humoral, cytotoxic T lymphocyte (CTL) immune responses, and two modes of transmission that are the classical virus-to-cell infection and the direct cell-to-cell transmission are investigated. The model incorporates three delays, including the delays of cell infection, virus production and activation of immune response. We first prove the well-posedness of the model, and calculate the biological existence of equilibria and the reproduction numbers, which contain virus infection, humoral immune response, CTL immune response, CTL immune competition, and humoral immune competition. Further, the threshold conditions for the local and global stability of the equilibria for infection-free, immune-free, antibody response, CTL response, and interior are established by utilizing linearization method and the Lyapunov functionals. The existence of Hopf bifurcation with immune delay as a bifurcation parameter is investigated by using the bifurcation theory. Numerical simulations are carried out to illustrate the theoretical results and reveal the effects of some key parameters on viral dynamics. [ABSTRACT FROM AUTHOR]

It is well known that dynamical systems are very useful tools to study viral diseases such as HIV, HBV, HCV, Ebola and Influenza. This paper focuses on a mathematical model of the cell-to-cell and the cell-free spread of HIV with both linear and nonlinear functional responses and logistic target cell growth. The reproduction number of each mode of transmission has been calculated and their sum has been considered as the basic reproduction number. Based on the values of the reproduction number, the local and global stabilities of the rest points are investigated. Choosing a suitable bifurcation parameter, some conditions for the occurrence of Hopf bifurcation are also obtained. Moreover, numerical simulations are presented to support the analytical results. Finally, to study the effect of the drug on the disease process, some control conditions are determined. Since two modes of transmission and both linear and nonlinear functional responses have been included in this manuscript, our obtained results are a generalization of those in the literature. Moreover, the results are obtained with weaker assumptions in comparison with the previous ones. [ABSTRACT FROM AUTHOR]

In recent decades, AIDS has been one of the main challenges facing the medical community around the world. Due to the large human deaths of this disease, researchers have tried to study the dynamic behaviors of the infectious factor of this disease in the form of mathematical models in addition to clinical trials. In this paper, we study a new mathematical model in which the dynamics of CD 4 + T-cells under the effect of HIV-1 infection are investigated in the context of a generalized fractal-fractional structure for the first time. The kernel of these new fractal-fractional operators is of the generalized Mittag-Leffler type. From an analytical point of view, we first derive some results on the existence theory and then the uniqueness criterion. After that, the stability of the given fractal-fractional system is reviewed under four different cases. Next, from a numerical point of view, we obtain two numerical algorithms for approximating the solutions of the system via the Adams-Bashforth method and Newton polynomials method. We simulate our results via these two algorithms and compare both of them. The numerical results reveal some stability and a situation of lacking a visible order in the early days of the disease dynamics when one uses the Newton polynomial. [ABSTRACT FROM AUTHOR]

The paper is focused on stochastic modelling of the process of transition of infected cells and virions of HIV-1 infection between two lymph nodes. The model is based on the following assumptions: (1) the duration of transition of infected cells and virions between two lymph nodes is set using a time-dependent function, (2) infected cells produce virions in the process of transition between two lymph nodes, (3) infected cells and virions may die when moving between two lymph nodes. The methods of the theory of branching random processes are used to study analytically the model variables. An algorithm for statistical modelling of the number of infected cells and virions in the second lymph node is presented. The results of computational experiments studying the distribution law of the number of virions produced by one infected cell depending on the duration of movement between two lymph nodes are presented. [ABSTRACT FROM AUTHOR]

In this paper, we propose and analyse a delayed HIV-1 model with both viral and cellular transmissions and virus waning. We obtain the threshold dynamics of the proposed model, characterized by the basic reproduction number R 0 . If R 0 < 1 , the infection-free steady state is globally asymptotically stable; whereas if R 0 > 1 , the system is uniformly persistent. When the delays are positive, we show that the intracellular delays in both viral and cellular infections may lead to stability switches of the infected steady state. Both analytical and numerical results indicate that if the effect of cell-to-cell transmission is ignored, then the risk of HIV-1 infection will be underestimated. Moreover, the viral load of model without virus waning is higher than the one of model with virus waning. These results highlight the important role of two ways of viral transmission and virus waning on HIV-1 infection. [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, an attempt has been made to study the global dynamical behavior of a viral dynamics model incorporating both the lytic and nonlytic immune responses. The global stability of the model is analyzed in terms of two threshold parameters, namely, basic reproduction number, R 0 and immune response reproduction number, R 1. The obtained results signify that the infection dies out if R 0 ≤ 1 and persists if R 0 > 1. We establish that the global dynamic behavior of the model has no concern with the efficacy of the nonlytic component. Numerical simulations are performed to support our theoretical findings and to investigate the effects of lytic and nonlytic components on the viral dynamics model. A comparison of two different viral infection models has been performed to illustrate the effect of viral replication inhibition through nonlytic effector mechanism on the infection dynamics. Moreover, a case study of HIV-1 infected humanized mice is presented and the result manifests that the model can fairly demonstrate the chronic stage of HIV-1 infection in humanized mice. • A viral dynamic model with lytic and nonlytic immune responses has been presented. • Global stability of the model is independent of the efficacy of nonlytic strength. • Inhibition of viral replication reduces the level of infected cells and virions. • The model fairly demonstrates the chronic HIV-1 infection in humanized mice. [ABSTRACT FROM AUTHOR]

This paper study the dynamical behavior of a general HIV-1 infection model under the effect of Highly active antiretroviral therapies (HAART). The model includes three types of infected cells (i) long-lived productively infected cells which live for long time and creat small amount of HIV-1 particles, (ii) latently infected cells which do not creat HIV-1 until they have been activated (iii) short-lived productively infected cells which live for long time and creat large amount of HIV-1. The model incorporates humoral immune response and general nonlinear forms for the incidence rate of infection, the generation and removal rates of all compartments. The nonnegativity and boundedness of the solutions of the model as well as global stability of the steady states are studied. The global stability are established using Lyapunov method. Using MATLAB we conduct some numerical simulations to confirm our results. [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]

The modern antiretroviral treatment of human immunodeficiency virus (HIV-1) infection has considerably lowered the incidence of opportunistic infections. With the exception of the most severe dementia manifestations, the incidence and prevalence of HIV-associated neurocognitive disorders (HAND) have not decreased, and HAND continues to be relevant in daily clinical practice. Now, HAND occurs in earlier stages of HIV infection, and the clinical course differs from that before the widespread use of combination antiretroviral treatment (cART). The predominant clinical feature is a subcortical dementia with deficits in the domains concentration, attention, and memory. Motor signs such as gait disturbance and impaired manual dexterity have become less prominent. Prior to the advent of cART, the cerebral dysfunction could at least partially be explained by the viral load and by virus-associated histopathological findings. In subjects where cART has led to undetectable or at least very low viral load, the pathogenic virus-brain interaction is less direct, and an array of poorly understood immunological and probably toxic phenomena are discussed. This paper gives an overview of the current concepts in the field of HAND and provides suggestions for the diagnostic and therapeutic management. [ABSTRACT FROM AUTHOR]

In this paper, we consider a four dimensional model of the human immunodeficiency virus-1 (HIV-1) with delay, which is an extension of some three dimensional models. We approach the treatment problem by adding two controllers to the system for inhibiting viral production. The optimal controller $$u_{1}$$ is considered for vaccine and $$u_{2}$$ for the drug. The Pontryagin maximum principle with delay is used to characterize these optimal controls. At the end, numerical results are presented to illustrate the optimal solutions. The validity of the model was confirmed by proper semi-quantitative simulation of some clinical data. The model was used to predict the possible beneficial effects of vaccine and anti-retroviral drug administration in HIV-1 disease. [ABSTRACT FROM AUTHOR]

Highly active antiretroviral therapy (HAART) reduces the viral burden in human immunodeficiency virus type 1 (HIV-1) infected patients. The paper addresses the problem of controlling the predator-prey like model of the interaction among CD4+T-cell, CD8+ T-cell, and HIV-1 by an external drug agency. By exploring the dynamic properties of the system, the original system is first regrouped into two subsystems, then a nonlinear global controller is presented by designing two controllers over two complementary zones: a local controller on a finite region and a global controller over its complement. The local controller is designed to guarantee nonnegativty, and avoids the problem of control singularity within the neighborhood of the origin Il. The complementary controller is designed via back stepping for both subsystems over the complementary region. The closed-loop system is globally stable at nominal values through the introduction of a novel bridging virtual control, and the resulting controller is singularity free and guarantees nonnegativity. In this paper, simulations are conducted in discrete-time with sampling time Ts to show the effectiveness of the proposed method. [ABSTRACT FROM AUTHOR]

In this paper, a delayed human immunodeficiency virus (HIV)-1 infection model with absorption and cytotoxic T lymphocytes (CTL) immune response is studied. By using suitable Lyapunov functionals and LaSalle's invariance principle, it is proved that if the basic reproductive ratio is less than unity, the infection-free equilibrium is globally asymptotically stable; if the immune response reproductive ratio is less than unity and the basic reproductive ratio is greater than unity, sufficient conditions are derived for the global stability of the CTL-inactivated infection equilibrium; if the immune response reproductive ratio is greater than unity, sufficient conditions are obtained for the global stability of the CTL-activated infection equilibrium. Numerical simulations are carried out to illustrate the theoretical results. [ABSTRACT FROM PUBLISHER]

In this paper, we introduce the stochasticity into an HIV-1 infection model with cytotoxic T lymphocytes (CTLs) immune response via the technique of parameter perturbation. We show that there is a positive solution as desired in any population dynamics. Then we analyze the long time behavior of this model. We obtain a sufficient condition for the stochastic asymptotic stability in the large of the infection-free equilibrium and give the conditions for the solution fluctuating around the two infection equilibria (one without CTLs being activated and the other with). Finally, we make simulations to conform to our analytical results. [ABSTRACT FROM AUTHOR]

Abstract: In this paper, an HIV-1 infection model with distributed intracellular delays is investigated, where the intracellular delays account for the time the target cells are contacted by the virus particles and the time the contacted cells become actively infected meaning that the contacting virions enter cells and the time the virus has penetrated into a cell and the time the new virions are created within the cell and are released from the cell, respectively. By analyzing the characteristic equations, the local stability of an infection-free equilibrium and a chronic-infection equilibrium of the model is established. By using suitable Lyapunov functionals and LaSalle’s invariance principle, it is proved that if the basic reproduction ratio is less than unity, the infection-free equilibrium is globally asymptotically stable; and if the basic reproduction ratio is greater than unity, the chronic-infection equilibrium is globally asymptotically stable. [Copyright &y& Elsevier]

Abstract: In this paper, an HIV-1 infection model with a saturation infection rate and an intracellular delay accounting for the time between viral entry into a target cell and the production of new virus particles is investigated. By analyzing the characteristic equations, the local stability of an infection-free equilibrium and a chronic-infection equilibrium of the model is established. By using suitable Lyapunov functionals and the LaSalle invariant principle, it is proved that if the basic reproduction ratio is less than unity, the infection-free equilibrium is globally asymptotically stable; if the basic reproduction ratio is greater than unity, the chronic-infection equilibrium is globally asymptotically stable. [Copyright &y& Elsevier]

Abstract: Based on some important biological meanings, a class of more general HIV-1 infection models with time delay is proposed in the paper. In the HIV-1 infection model, time delay is used to describe the time between infection of uninfected target cells and the emission of viral particles on a cellular level as proposed by Herz et al. [A.V.M. Herz, S. Bonhoeffer, R.M. Anderson, R.M. May, M.A. Nowak, Viral dynamics in vivo: Limitations on estimates of intracellular delay and virus decay, Proc. Natl. Acad. Sci. USA 93 (1996) 7247–7251]. Then, the effect of time delay on stability of the equilibria of the HIV-1 infection model has been studied and sufficient criteria for local asymptotic stability of the infected equilibrium and global asymptotic stability of the viral free equilibrium are given. [Copyright &y& Elsevier]

This paper reports the results of the cross-sectional phase of a long-term follow-up investigation, carried out on a sample representative of the broad population of HIV-1 infected patients, with the objective of evaluating the possible neurocognitive effects of zidovudine and 2′, 3′-dideoxyinosine, compared to a group of people who refused antiretroviral therapy. The sample was composed of 88 people, 42 of whom were treated with ZDV at a daily dose of 500–600 mg, 19 with ddI at a daily dose of 400 mg, and 27 with no therapy. To assess the relevance of different antiretroviral therapies on cognitive performance adjusting for demographic and clinical characteristics, a stepwise logistic regression analysis was performed with neuropsychological performance as the dependent variable and age, education, sex, at-risk behaviour, CD4 count, presence of prominent depressive and anxious symptoms, HIV-1 serostatus and type of antiretroviral treatment as independent variables. The results confirm that people with AIDS and AIDS-related complex treated with ZDV and ddI show a better neuropsychological performance when compared to non-treated patients. By examining the mean performance on each of the previous neuropsychological tests, we found that the most impaired functions in untreated patients were related to short-term memory, long-term memory, vocational competence, and ultimate adjustment. [ABSTRACT FROM AUTHOR]