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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]

Aim and Objective: HIV (Human Immunodeficiency Virus) has been reported to weaken the immune system by binding to CD4+ receptor of T lymphocytes, thereby making the affected individual to become more susceptible to several microbial infections leading to life threatening problems. Recent literature indicate there is promsing advancement in identifying drug targets through CD4+ receptor binding capabilities with its ligand. The main purpose of this paper was to study the various molecular interactions of HIV to other molecules like receptors CD4+ and also co-receptors like CCR5 and CXCR4. Materials and Required: The molecules are going to be modeled by using software known as Swiss PDB viewer. The first objective is to get the FASTA sequence from the NCBI website. Then we need to paste the sequence onto the Swiss PDB viewer. Conclusion: The requierd protein/molecule is modeled. We are going to follow this method to obtain templates and modles for the following molecukles: HIV, GP120, CCR5 and CXCR4. [ABSTRACT FROM AUTHOR]

In this paper, we propose and analyze an HIV dynamics model. The model can be seen as a generalization of many HIV dynamics models presented in the literature since it incorporates (i) two classes of target cells, CD4+ T cells and macrophages, (ii) two types of infected cells, short-lived infected cells and the long-lived chronically infected cells, (iii) intracellular discrete delays, (iv) reverse transcriptase inhibitors (RTIs) drugs with different drug efficacies on CD4+T cells and macrophages. The incidence rate of infection is represented by a general function. A bifurcation parameter, known as the basic reproduction number, R0 is derived. We established a set of conditions on the general function which are sufficient to determine the global dynamics of the model. Using Lyapunov functionals and LaSalle's invariance principle, the global asymptotic stability of the two equilibria of the model is obtained. An example is presented and some numerical simulations are conducted in order to illustrate the dynamical behavior. [ABSTRACT FROM AUTHOR]

In this paper, we construct an HIV infection model which includes latent infection, logistic growth for healthy CD4 T-cells, and antiretroviral therapy. We obtain the global asymptotic stability of the uninfected equilibrium by constructing a Lyapunov function, and we give a sufficient condition for the local asymptotic stability of the infected equilibrium. We also use the latin hypercube sampling technique to identify the key parameters in determining the stability of the infected equilibrium. By numerical simulations, we observe that the model without logistic growth would underestimate the number of infectious virions, while the model without latent infection would overestimate the number of infectious virions. [ABSTRACT FROM AUTHOR]

Based on some important biological meanings, we propose a class of HIV infection models incorporating both classical cell-free virus diffusion and direct cell-to-cell transmission. According to recent studies, the direct cell-to-cell transfer of HIV is a significantly more efficient mode of retroviral dissemination. In the first part of our analysis, we show that our model possesses non-negative solutions. Then, we derive sufficient conditions for the asymptotic stability of equilibriums. The analytical solutions are verified by simulation results. At the end of the paper, some important conclusions are given. [ABSTRACT FROM AUTHOR]

This paper analyzes the main trend of the development of acquired immunodeficiency syndrome (AIDS) vaccines in recent years. Designing an HIV-1 vaccine that provides robust protection from HIV-1 infection remains a challenge despite many years of effort. Therefore, we describe the receptor binding domain of gp120 as a target for developing AIDS vaccines. And we recommend some measures that could induce efficiently and produce cross-reactive neutralizing antibodies with high binding affinity. Those measures may offer a new way of the research and development of the potent and broad AIDS vaccines. [ABSTRACT FROM AUTHOR]

Abstract: The strategies of structured treatment interruptions (STIs) of antiretroviral therapies have been proposed for clinical management of HIV infected patients, but clinical studies on STIs failed to achieve a consistent conclusion for this strategy. To evaluate the STI strategies, in particular, CD4+ T cell count-guided STIs, and explain these controversial conclusions from different clinical studies, in this paper we propose to use piecewise HIV virus dynamic models to quantitatively explore the STI strategies and investigate their dynamic behaviors. Our analysis results indicate that CD4+ T cell counts can be maintained above a safe level using the STI with a single threshold or a threshold window. Numerical simulations show that the CD4+ T cell counts either fluctuate or approach a stable level for a patient, depending on the prescribed upper or lower threshold values. In particular, the CD4+ T cell counts can be stabilized at a desired level if the threshold policy control is applied. The durations of drug-on and drug-off are very sensitive to the prescribed upper or lower threshold levels, which possibly explains why the on–off strategy with fixed schedule or an STI strategy with frequent switches are associated with the high rate of failure. Our findings suggest that it is critical to carefully choose the thresholds of CD4+ T cell count and individualize the STIs for each individual patient based on initial CD4+ T cell counts. [Copyright &y& Elsevier]

While antiretroviral drugs can drive HIV to undetectably low levels in the blood, eradication is hindered by the persistence of long-lived, latently infected memory CD4 T cells. Immune activation therapy aims to eliminate this latent reservoir by reactivating these memory cells, exposing them to removal by the immune system and the cytotoxic effects of active infection. In this paper, we develop a mathematical model that investigates the use of immune activation strategies while limiting virus and latent class rebound. Our model considers infection of two memory classes, central and transitional CD4 T cells and the role that general immune activation therapy has on their elimination. Further, we incorporate ways to control viral rebound by blocking activated cell proliferation through anti proliferation therapy. Using the model, we provide insight into the control of latent infection and subsequently into the long term control of HIV infection. [ABSTRACT FROM AUTHOR]

The requirements for the eradication of HIV in infected individuals are unknown. Intermittent administration of the immune activator interleukin-2 (IL-2) in combination with highly-active anti-retroviral therapy (HAART) has been suggested as an effective strategy to realize long-term control of HIV replication in vivo . However, potential latent virus reservoirs are considered to be a major impediment in achieving this goal. In this paper, a new mathematical model is designed and used to monitor the interactions between HIV, CD4+ T-cells, CD8+ T-cells, productively infected and latently infected CD4+ T-cells, and to evaluate therapeutic strategies during the first 3 years of HIV infection. The model shows that current anti-HIV therapies, including intermittent IL-2 and HAART, are insufficient in achieving eradication of HIV. However, it suggests that the HIV eradication may indeed be theoretically feasible if such therapy is administered continuously (without interruption) under some specified conditions. These conditions may realistically be achieved using an agent (such as a putative anti-HIV vaccine) that brings about a concomitant increase in the proliferation of HIV-specific CD4+ T- and CD8+ T-cells and the differentiation of CD8+ T-cells into anti-HIV cytotoxic T lymphocytes (CTLs). [ABSTRACT FROM AUTHOR]

Discusses the abstract of the paper 'The Reservoir for HIV-1 in Human Peripheral Blood is a T Cell That Maintains Expression of CD4,' by Steven M. Schniltman et al published in an issue of the periodical 'Science.'