A stochastic model for internal HIV dynamics

In this paper we analyse a stochastic model representing HIV internal virus dynamics. The stochasticity in the model is introduced by parameter perturbation which is a standard technique in stochastic population modelling. We show that the model established in this paper possesses non-negative solutions as this is essential in any population dynamics model. We also carry out analysis on the asymptotic behaviour of the model. We approximate one of the variables by a mean reverting process and nd out the mean and variance of this process. Numerical simulations conclude the paper

Mathematical modelling of internal HIV dynamics

We study a mathematical model for the viral dynamics of HIV in an infected individual in the presence of HAART. The paper starts with a literature review and then formulates the basic mathematical model. An expression for R0, the basic reproduction number of the virus under steady state application of HAART, is derived followed by an equilibrium and stability analysis. There is always a disease-free equilibrium (DFE) which is globally asymptotically stable for R0 1 then some simulations will die out whereas others will not. Stochastic simulations suggest that if R0 > 1 those which do not die out approach a stochastic quasi-equilibrium consisting of random uctuations about the non-trivial deterministic equilibrium levels, but the amplitude of these uctuations is so small that practically the system is at the non-trivial equilibrium. A brief discussion concludes the paper

Hopf Bifurcation and Stability of Periodic Solutions for Delay Differential Model of HIV Infection of CD4 +

This paper deals with stability and Hopf bifurcation analyses of a mathematical model of HIV infection of CD4+ T-cells. The model is based on a system of delay differential equations with logistic growth term and antiretroviral treatment with a discrete time delay, which plays a main role in changing the stability of each steady state. By fixing the time delay as a bifurcation parameter, we get a limit cycle bifurcation about the infected steady state. We study the effect of the time delay on the stability of the endemically infected equilibrium. We derive explicit formulae to determine the stability and direction of the limit cycles by using center manifold theory and normal form method. Numerical simulations are presented to illustrate the results

Antiretroviral therapy of HIV infection using a novel optimal type-2 fuzzy control strategy

Abstract The human immunodeficiency virus (HIV), as one of the most hazardous viruses, causes destructive effects on the human bodies' immune system. Hence, an immense body of research has focused on developing antiretroviral therapies for HIV infection. In the current study, we propose a new control technique for a fractional-order HIV infection model. Firstly, a fractional model of the HIV model is investigated, and the importance of the fractional-order derivative in the modeling of the system is shown. Afterward, a type-2 fuzzy logic controller is proposed for antiretroviral therapy of HIV infection. The developed control scheme consists of two individual controllers and an aggregator. The optimal aggregator modifies the output of each individual controller. Simulations for two different strategies are conducted. In the first strategy, only reverse transcriptase inhibitor (RTI) is used, and the superiority of the proposed controller over a conventional fuzzy controller is demonstrated. Lastly, in the second strategy, both RTI and protease inhibitors (PI) are used simultaneously. In this case, an optimal type-2 fuzzy aggregator is also proposed to modify the output of the individual controllers based on optimal rules. Simulations results demonstrate the appropriate performance of the designed control scheme for the uncertain system

Stability and Feedback Stabilization of HIV Infection Model with Two Classes of Target Cells

We study the stability and feedback stabilization of the uninfected steady state of a human immunodeficiency virus (HIV) infection model. The model is a 6-dimensional nonlinear ODEs that describes the interaction of the HIV with two classes of target cells, CD4+ T cells and macrophages, and takes into account the Cytotoxic T Lymphocytes (CTLs) immune response. Lyapunov function is constructed to establish the global asymptotic stability of the uninfected steady state of the model. In a control system framework, the HIV infection model incorporating the effect of Highly Active AntiRetroviral Therapy (HAART) is considered as a nonlinear control system with drug dose as control input. We developed treatment schedules for HIV-infected patients by using Model Predictive Control (MPC-)based method. The MPC is constructed on the basis of an approximate discrete-time model of the HIV infection model. The MPC is applied to the stabilization of the uninfected steady state of the HIV infection model. Besides model inaccuracies that HIV infection model suffers from, some disturbances/uncertainties from different sources may arise in the modelling. In this work the disturbances are modelled in the HIV infection model as additive bounded disturbances. The robustness of the MPC against small model uncertainties or disturbances is also shown

Mathematical modelling of low HIV viral load within Ghanaian population

Comparatively, HIV like most viruses is very minute, unadorned organism which cannot reproduce unaided. It remains the most deadly disease which has ever hit the planet since the last three decades. The spread of HIV has been very explosive and mercilessly on human population. It has tainted over 60 million people, with almost half of the human population suffering from AIDS related illnesses and death finally. Recent theoretical and computational breakthroughs in delay differential equations declare that, delay differential equations are proficient in yielding rich and plausible dynamics with reasonable parametric estimates. This paper seeks to unveil the niche of delay differential equation in harmonizing low HIV viral haul and thereby articulating the adopted model, to delve into structured treatment interruptions. Therefore, an ordinary differential equation is schemed to consist of three components such as untainted CD4+ T-cells, tainted CD4+ T-cells (HIV) and CTL. A discrete time delay is ushered to the formulated model in order to account for vital components, such as intracellular delay and HIV latency which were missing in previous works, but have been advocated for future research. It was divested that when the reproductive number was less than unity, the disease free equilibrium of the model was asymptotically stable. Hence the adopted model with or without the delay component articulates less production of virions, as per the decline rate. Therefore CD4+ T-cells in the blood remains constant at 1/3, hence declining the virions level in the blood. As per the adopted model, the best STI practice is intimated for compliance.Mathematical SciencesPh.D. (Applied Mathematics

Contributions to the Mathematical Systems Medicine of Antimicrobial Therapy and Genotype-Phenotype Inference.

The following summary of my publications describes the main ideas in the corresponding research articles and clarfifies my contribution in multi-author publications. I decided to apply for habilitation according to x2.I.1.(c) of the Habilitationsordnung (this path is usually referred as Kumulative Habilitation"). I selected 13 first- or last author publications for this habilitation that concern contributions to the mathematical systems medicine of antiviral therapy [tMH10, tMS+11, FtK+11, tMMS12, DSt12, DWSt15, Dt16, DSt16, DDKt18, DSD+19, DDKt19], as well as inference of genotype-phenotype associations [SDH+15, SSJ+18]. The selected publications represent my major contributions in this research eld since submitting my doctoral thesis in September 2009

Adherence to antiretroviral combination therapy in children : what a difference half a day makes...

Adherence to antiretroviral combination therapy in children. What a difference half a day makes____ has explored the opportunities to support evidence generation and extrapolation across populations, with special focus on the selection of the dose, the optimisation of dosing regimens and the impact of patient behaviour towards antiretroviral treatment. A model-based approach for the evaluation of covariate effects and forgiveness of non-adherence, which may allow simplification of current dosing regimens taking into consideration inadequate compliance and its implication for efficacy and drug resistance, has been proposed. In conjunction with clinical trial simulations, this thesis addressed the possibility to evaluate relevant clinical scenarios and predict treatment outcome of simplified dosing regimens, taking into account the differences in the patterns of drug intake and the pharmacokinetic-pharmacodynam ic properties of antiretroviral drugs.UBL - phd migration 201