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Data clustering is a thoroughly studied data mining issue. As the amount of information being analyzed grows exponentially, there are several problems with clustering diagnostic large datasets like the monitoring, microbiology, and end results (SEER) carcinoma feature sets. These traditional clustering methods are severely constrained in terms of speed, productivity, and adaptability. This paper summarizes the most modern distributed clustering algorithms, organized according to the computing platforms used to process vast volumes of data. The purpose of this work was to offer an optimized distributed clustering strategy for reducing the algorithm's total execution time. We obtained, preprocessed, and analyzed clinical SEER data on liver cancer, respiratory cancer, human immunodeficiency virus (HIV)-related lymphoma, and lung cancer for large-scale data clustering analysis. Three major contributions and their effects were covered in this paper: To begin, three current Pyspark distributed clustering algorithms were evaluated on SEER clinical data using a simulated New York cancer dataset. Second, systemic inflammatory response syndrome (SIRS) model inference was done and described using three SEER cancer datasets. Third, employing lung cancer data, we suggested an optimized distributed bisecting k -means method. We have shown the outcomes of our suggested optimized distributed clustering technique, demonstrating the performance enhancement. [ABSTRACT FROM AUTHOR]

AIDS is a chronic infectious disease that has been having a major impact on human health and social stability. In this paper, based on the deterministic SIATR model, a stochastic SIATR model is developed to account for the spread of AIDS by introducing the Ornstein–Uhlenbeck process. First, the existence and uniqueness of the global positive solution of the model are investigated. Second, a threshold R0E is set: when R0E < 1, the disease will become extinct; when R0E > 1, the disease will persist. Then, it is shown that there exists a stationary distribution for the model when R0E > 1. On this basis, we derive the exact expression for the probability density function of the model in the neighborhood of the quasi-equilibrium state. Finally, the results of the previous proof are verified by several numerical simulations. [ABSTRACT FROM AUTHOR]

The primary objective of this paper is to conduct an in-depth analysis of the intricacies inherent in a gender-structured model depicting the dynamics of HIV–TB coinfection. The model is articulated through a set of nonlinear fractional-order differential equations. Our focus is on elucidating the stability characteristics around equilibrium points, employing advanced fractional stability techniques. We leverage sensitivity analysis as a powerful tool to discern the specific model parameters exerting significant influence on the transmission and control of the coinfection, as gauged by the basic reproduction number. Through this, we aim to identify key factors that drive the spread or containment of the dual affliction. Furthermore, we delve into the realm of optimization by formulating a fractional optimal control problem. The objective is to design and implement two control strategies that effectively mitigate the prevalence of coinfection, demonstrating a state of perfect protection. Notably, our findings reveal that the implementation of control measures at a rate exceeding 80% suffices to eliminate the infection entirely. We anticipate that the insights garnered from this research will prove instrumental for policymakers in crafting strategic interventions to curtail the tragic impact of HIV–TB coinfection. Our scientifically grounded study serves as a foundation upon which comprehensive plans can be devised to stem the devastating consequences of this dual health challenge. [ABSTRACT FROM AUTHOR]

Reverse transcriptase (RT) and integrase (IN) are two pivotal enzymes in HIV-1 replication. RT converts the single-stranded viral RNA genome into double-stranded DNA and IN catalyzes the integration of viral double-stranded DNA into host DNA. Currently, dual inhibitors of HIV-1 RT and IN have become a hotspot in new anti-HIV drug research and development. A dual inhibitor of HIV-1 RT/IN does the same thing as the two independent drugs would do. In this paper, we develop a mathematical model comprising a system of nonlinear differential equations describing HIV-1 RT/IN catalyzed biochemical reactions based on Michaelis–Menten enzyme kinetic reaction. In the formulated model we incorporate HIV-1 RT/IN dual inhibitor which simultaneously works as a non-nucleoside RT inhibitor and IN inhibitor. To examine the efficacy of HIV-1 RT/IN dual inhibitor in the treatment of HIV-1 infection, we have introduced a one-dimensional impulsive differential equation model and determined an effective dosing regimen for applying the inhibitor numerically. Furthermore, the exact closed form solution of the impulsive differential equation model is carried out by using the Lambert W function and the local stability of the periodic solution is also obtained analytically. The results obtained from analytical as well as numerical studies provide a basic idea to investigate the minimum dose with the highest efficacy for administering HIV-1 RT/IN dual inhibitors to prevent HIV-1 infection. [ABSTRACT FROM AUTHOR]

This paper is concerned with the minimal wave speed of nonconstant traveling wave solutions in an HIV-1 virus integrodifference system. Here, the traveling wave solution models the spatial spreading process of infected cells and virus. When the basic reproduction ratio of the corresponding ordinary differential system or difference system is larger than one, we establish the existence of nonconstant traveling wave solutions if the wave speed is not less than a threshold, and if the speed is smaller than the threshold, we prove the nonexistence of nonconstant traveling wave solutions. Moreover, when the basic reproduction ratio of the corresponding ordinary differential system or difference system is not larger than one, we also confirm the nonexistence of nonconstant traveling wave solutions. [ABSTRACT FROM AUTHOR]

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]

The human immunodeficiency virus (HIV) is a major global public health issue and causes millions of deaths around the globe. The most severe phase of HIV infection is known as AIDS. In recent years, a number of mathematical models based on classical integer-order derivative have been developed to analyze the insight dynamics of HIV/AIDS. This paper presents the transmission dynamics of HIV/AIDS using fractional order (FO) and a fractal-fractional order compartmental model with the power-law kernel. In the first phase, the proposed model is formulated using the Caputo-type fractional derivative. The basic properties such as the solution positivity and existence as well as uniqueness of the fractional model are presented. The equilibria and the basic reproductive number ℛ 0 are evaluated. Further, using fractional stability concepts the stability of the model (both local and global) around the equilibrium is presented in the disease-free case. In addition, the fractional model is solved numerically, and the graphical results with many values of q 1 are shown. In the second phase, the concept of a fractal-fractional (FF) operator is applied to obtain a more generalized model that addresses the dynamics of HIV/AIDS. The uniqueness and existence of the solutions of the FF-based model are shown via the Picard–Lindelof approach while the modified Adams–Bashforth method is utilized to present the numerical solution. Detailed numerical simulations are presented for various values fractional as well as the fractal orders, q 1 and q 2 , respectively. The graphical results reveal that the FF-based model provides biologically more feasible results than the models in fractional and classical integer-order cases. [ABSTRACT FROM AUTHOR]

In the course of reverse transcription, drug-sensitive strain can mutate to a drug-resistant one. Cell-to-cell transmission is proved to be more efficient than virus-to-cell infection. The population of Cytotoxic T Lymphocytes (CTLs) can be divided into CTL precursors and CTL effectors. Naive CTL precursors are those that never have contacted antigen, circulating around the body. Once the host is infected, CTL precursors (CTLp) begin to proliferate and differentiate into CTL effectors (CTLe), which have antiviral activity. In this paper, we study an HIV model with drug-sensitive and drug-resistant mixed strains, CTLp and CTLe, both viral and cellular infections. The basic reproduction ratios for each strain are derived and the stability of each feasible equilibrium is analyzed by using Routh–Hurwitz criteria. The periodic solutions may occur near the equilibrium with CTL immune response via Hopf bifurcation. By using normal form theory, we find more information about the limit cycles, such as the amplitude, phase and stability. [ABSTRACT FROM AUTHOR]

The main target of both human immunodeficiency virus type 1 (HIV-1) and human T-lymphotropic virus type I (HTLV-I) is the CD4+ T cell which is considered the key player in the immune system. Moreover, HIV-1 has another target that is the macrophages. The present paper aims to formulate and develop a mathematical model to analyze the interaction of two viruses, HIV-1 and HTLV-I with the immune system. We determine a bounded domain for the concentrations of the model's compartments. We discuss the dynamical behavior of the model and analyze the existence and stability of the system's steady states. The global asymptotic stability of all steady states is proven by utilizing the Lyapunov method. We also demonstrate the dynamical behavior of the system numerically. The significant impact of macrophages on the HTLV-I/HIV-1 co-infection dynamics is discussed. Our developed model will contribute to the understanding of HTLV-I/HIV-1 co-infection dynamics and help to choose different treatment strategies against HIV-1 and HTLV-I. [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, an HIV infection model with eclipse phase, humoral immune response and immunological delay has been discussed. By studying the characteristic equations of the model, the local stability analysis of various equilibrium points has been explored. Treating the delay as the bifurcation parameter, it has been shown that the delay can destabilize the stability of the infected steady-state leading to Hopf bifurcation and periodic solutions. By using Lyapunov functionals and LaSalle's invariance principle, the global stability analysis of the boundary equilibrium points has also been explored. It has also been shown numerically that the inclusion of the drug therapy in the model generates sporadic outbursts of virus called viral blips. In the end, numerical simulations have been employed to justify the analytical results proved in the paper. Biologically, the proposed model can explain the presence of viral blips in the system, during the introduction of HAART, as observed in the HIV-infected patient. These blips could mark the viral advancement in the system, thus resulting in complete immunological failure. One of the reasons for these viral blips can be the presence of delay in the activation of immunological response. But the development of drug-resistive virus could also be the reason for this sudden rise in viral loads. Moreover, the incorporation of the delay in the model generates oscillations and periodicity in the model, thus validating the long latency period seen in most HIV-infected patients. Also, a longer delay in the activation of immune response marks a viral advancement in the viral timeline resulting in viral blips, which signify the evolution of the virus. [ABSTRACT FROM AUTHOR]

In this paper, we present a fractional model for the HIV/AIDS epidemic and incorporate into the model control parameters of pre-exposure prophylaxis (PrEP), behavioral change and antiretroviral therapy (ART) aimed at controlling the spread of diseases. We prove the local and global asymptotic stability of disease-free and endemic equilibria of the model. We present a general fractional optimal control problem (FOCP) with free terminal time and develop the Adapted Forward-Backward Sweep method for numerical solving of the FOCP. Necessary conditions for a state/control/terminal time triplet to be optimal are obtained. The results show that the use of all controls increases the life expectancy of HIV-treated patients with ART and remarkably increases the number of people undergoing PrEP and changing their sexual habits. Also, when the derivative order α (0. 4 5 ≤ α ≤ 1) limits to 1, the value of optimal terminal time increases while the value of objective functional decreases. [ABSTRACT FROM AUTHOR]

This paper presents a comprehensive analysis, carried out by the molecular dynamics (MD) simulations, of the vibrations of silicon nanowire (SiNW) resonators, having diverse applications including biological and medical fields. The chosen approach allows us to obtain a better understanding of the nanowire (NW) materials' characteristics, providing a more detailed insight into the behavior of nanostructures, especially when the topic of interest is relevant to their dynamics, interatomic interactions, and atoms trajectories' prediction. We first simulate a SiNW to study its frequency of vibrations using MD simulations. Then, we add a molecule of human immunodeficiency virus as an example to investigate the potential of the SiNW resonator for the detection of tiny bio-objects. The developed technique and its application to the detection of tiny objects, such as viruses, are discussed in the context of several key effects pertinent to the design of SiNW. [ABSTRACT FROM AUTHOR]

In this paper, we mainly investigate an infected-age structured HIV model with logistic growth for target cells, which simultaneously takes the latent factor and different transmission modes into consideration. On the basis of integrated semigroup theory and Hopf bifurcation theory for semilinear equations in a nondense domain, we reach a conclusion that the system undergoes a Hopf bifurcation around the positive equilibrium, which implies that there exists a nontrivial periodic oscillation phenomenon when the Hopf bifurcation parameter τ passes through some critical values. Namely, the HIV infection will periodically erupt when the mature period τ crosses the critical value τ k (k = 0 , 1 , 2 , ...), that is, HIV virus will always survive in the patient's body. In order to verify the fact that the biological maturation period τ does play an essential role in our system, we also offer the relevant numerical simulation results by selecting several decisive parameters. [ABSTRACT FROM AUTHOR]

In this paper, we analyze a higher-order stochastically perturbed multigroup staged-progression model for the transmission of HIV with saturated incidence rate. We obtain sufficient conditions for the existence and uniqueness of an ergodic stationary distribution of positive solutions to the system by establishing a suitable stochastic Lyapunov function. In addition, we make up adequate conditions for complete eradication and wiping out the infectious disease. In a biological interpretation, the existence of a stationary distribution implies that the disease will prevail and persist in the long term. Finally, examples and numerical simulations are introduced to validate our theoretical results. [ABSTRACT FROM AUTHOR]

Individuals infected by human immunodeficiency virus (HIV) are under oxidative stress due to the imbalance between reactive oxygen species (ROS) production and elimination. This paper presents a mathematical model with the cytotoxic T lymphocytes (CTL) immune response to examine the role of ROS in the dynamics of HIV infection. We classify the equilibria of the model and study the stability of these equilibria. Numerical simulations show that incorporating ROS and CTL immune response into the model leads to very rich dynamics, including bistable phenomena and periodic solutions. Although the current antiretroviral therapy can suppress viral load to the undetectable level, it cannot eradicate the virus. A high level of ROS may be a factor for HIV persistence in patients despite suppressive therapy. These results suggest that oxidative damage and anti-oxidant therapy should be considered in the study of HIV infection and treatment. [ABSTRACT FROM AUTHOR]

In this paper, we formulate an age-structured HIV model, in which the influence of humoral immunity and the infection age of the infected cells are considered. The model is governed by three ordinary differential equations and two first-ordered partial differential equations and admits three equilibria: disease-free, immune-inactivated and immune-activated equilibria. We introduce two important thresholds: the basic reproduction number R 0 and immune-activated reproduction number R 1 and further show the global stability of above three equilibria in terms of R 0 and R 1 , respectively. The numerical simulations are presented to illustrate our results. [ABSTRACT FROM AUTHOR]

Human immunodeficiency virus (HIV) and human T-lymphotropic virus type I (HTLV-I) are two retroviruses that infect the susceptible CD 4 + T cells. It is known that HIV and HTLV-I have in common a way of transmission through direct contact with certain body fluids related to infected individuals. Therefore, it is not surprising that a mono-infected person with one of these viruses can be co-infected with the other virus. In the literature, a great number of mathematical models has been presented to describe the within-host dynamics of HIV or HTLV-I mono-infection. However, the within-host dynamics of HIV/HTLV-I co-infection has not been modeled. In this paper, we develop a new within-host HIV/HTLV-I co-infection model. The model includes the impact of Cytotoxic T lymphocytes (CTLs) immune response, which is important to control the progression of viral co-infection. The model describes the interaction between susceptible CD 4 + T cells, silent HIV-infected cells, active HIV-infected cells, silent HTLV-infected cells, Tax-expressing HTLV-infected cells, free HIV particles, HIV-specific CTLs and HTLV-specific CTLs. We first show the nonnegativity and boundedness of the model's solutions and then we calculate all possible equilibria. We derive the threshold parameters which govern the existence and stability of all equilibria of the model. We prove the global asymptotic stability of all equilibria by utilizing Lyapunov function and LaSalle's invariance principle. We have presented numerical simulations to illustrate the effectiveness of our main results. In addition, we discuss the effect of HTLV-I infection on the HIV-infected patients and vice versa. [ABSTRACT FROM AUTHOR]

In this paper, a delayed HIV/AIDS epidemic model with treatment and spatial diffusion is introduced. By analyzing the corresponding characteristic equations, the local stability of a disease-free steady state and an endemic steady state is discussed. By using the cross-iteration method and Schauder's fixed point theorem, we reduce the existence of traveling waves to the existence of a pair of upper–lower solutions. By constructing a pair of upper–lower solutions, we derive the existence of a traveling wave solution connecting the disease-free steady state and the endemic steady state. It is shown that the existence of traveling waves of the proposed HIV/AIDS epidemic model is fully determined by the basic reproduction number and the minimal wave speed. Finally, numerical simulations are performed to show the feasibility and effectiveness of the theoretical results. [ABSTRACT FROM AUTHOR]

In this paper, a nonlinear population model for HIV-TB co-infection has been proposed. The model is incorporated with the effect of early and late initiation of HIV treatment in co-infectives already on TB treatment, on the occurrence of Immune Reconstitution Inflammatory syndrome (IRIS). A 15-dimensional (15D) mathematical model has been developed in this study. We begin with considering constant treatment rates and thereafter, proceed to time-dependent treatment rates for co-infectives as control parameters. The basic reproduction number, a threshold quantity, corresponding to each HIV and TB sub-model has been computed in case of constant controls. With constant values of control parameters, mathematical analysis shows the existence and local stability of the disease-free equilibrium point and the endemic equilibrium point for the model. Together with time-dependent parameters, an optimal control problem is introduced and solved using Pontryagin's maximum principle with an objective to minimize the number of infectives and disease induced deaths along with the cost of treatment. Numerical simulations are performed to examine the effect of reproduction numbers on control profiles and to identify, the ideal combination of treatment strategies which provides minimum burden on a society. Numerical results imply that if both HIV and TB are endemic in the population, then in order to bring in minimum burden from the co-infection, optimal control efforts must be enforced rather than constant treatment rate. [ABSTRACT FROM AUTHOR]

In this paper, we develop mathematical models that include impairment of B-cell functions in order to study HIV dynamics. Two forms of the incidence rate have been considered, bilinear and general nonlinear. Three types of infected cells have been incorporated into the models, namely latently infected, short-lived productively infected and long-lived productively infected. The models have at most two equilibria, whose existence is characterized by means of the basic reproduction number R 0 . The global stability of each equilibrium is proven by using the Lyapunov method. The effects of impairment of B-cell functions and of antiviral treatment on the human immunodeficiency virus (HIV) dynamics are studied. We have shown that if the functions of B-cell are impaired, then the concentration of HIV increases in the plasma. Moreover, we have determined the minimal drug efficacy which is required to reduce the concentration of HIV particles to a lower level. We have shown that a more accurate computation of drug efficacy can be performed by using our proposed model. Our theoretical results are illustrated by means of numerical simulations. [ABSTRACT FROM AUTHOR]

In this paper, we incorporate immune systems into an HIV model, which considers both logistic target-cell proliferation and viral cell-to-cell transmission. We study the dynamics of this model including the existence and stability of equilibria. Based on the existence of equilibria, we focus on the backward bifurcation and forward bifurcation. Considering the stability of equilibria, Hopf bifurcation is discussed by identifying the basic reproduction number R 0 as bifurcation parameter. The direction and stability of Hopf bifurcation are investigated by computing the first Lyapunov exponent. Specially, the effects of immune response on the basic reproduction number R 0 and viral dynamics are addressed by deriving the sensitivity analysis. As a result, we find that the removal rate of infected cells by cytotoxic T lymphocytes (CTLs), γ 1 , is the predominant factor of R 0 . However, we conclude from numerical results that it is unfeasible to decrease R 0 by increasing the value of γ 1 constantly. Numerical simulation is also presented to demonstrate the applicability of the theoretical predictions. These dynamics are investigated by the proposed model to point out the importance and complexity of immune responses in fighting HIV replication. [ABSTRACT FROM AUTHOR]

In this paper, we define the basic concept of triangular neutrosophic cubic hesitant fuzzy number and their properties. We develop a triangular neutrosophic cubic hesitant fuzzy ordered weighted arithmetic averaging (TNCHFOWAA) operator and a triangular neutrosophic cubic hesitant fuzzy ordered weighted geometric averaging (TNCHFOWGA) operator to aggregate triangular neutrosophic cubic hesitant fuzzy number (TNCHFN) information and investigate their properties. Furthermore, a multiple attribute decision-making method based on the TNCHFOWAA operator and triangular neutrosophic cubic hesitant fuzzy ordered weighted geometric (TNCHFOWG) operator and the score function of TNCHFN is established under a TNCHFN environment. Finally, an illustrative example of investment alternatives is given to demonstrate the application and effectiveness of the developed approach. [ABSTRACT FROM AUTHOR]

In this paper, we present a general formulation for a fractional optimal control problem (FOCP), in which the state and co-state equations are given in terms of the left fractional derivatives. We develop the forward–backward sweep method (FBSM) using the Adams-type predictor–corrector method to solve the FOCP. We present a fractional model for transmission dynamics of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) with treatment and incorporate three control efforts (effective use of condoms, ART treatment and behavioral change control) into the model aimed at controlling the spread of HIV/AIDS epidemic. The necessary conditions for fractional optimal control of the disease are derived and analyzed. The numerical results show that implementing all the control efforts increases the life time and the quality of life those living with HIV and decreases significantly the number of HIV-infected and AIDS people. Also, the maximum levels of the controls and the value of objective functional decrease when the derivative order α limits to 1 (0. 7 ≤ α < 1). In addition, the effect of the fractional derivative order α (0. 7 ≤ α < 1) on the spread of HIV/AIDS epidemic and the treatment of HIV-infected population is investigated. The results show that the derivative order α can play the role of using ART treatment in the model. [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]

Human immunodeficiency virus (HIV) emerged as one of the most serious health issues of the modern era. Till date, it challenges the scientists working in the fields related to its prevention, least spread and eradication. It affects not only the person suffering from it but also the communities and their economies. Mathematical modeling is one of the ways to explore the possibilities of prediction (and control) strategies for contagious deceases. In this paper, we have tried to extend the scope of a currently available prediction model for a continuous time span. For this purpose, an analytical investigation of the system of nonlinear differential equations, governing the HIV infection of CD4T-cells, is carried out. A new emerging analytical technique Optimal Variational Iteration Method (OVIM) has been used to obtain an analytical and convergent solution. Analytical solutions are continuous solutions that can be used to predict the phenomena without the involvement of interpolation or extrapolation errors. On the other hand, their use in the derived equations, depending upon solution itself, is far easier than the numerical solutions. We have presented the error analysis and the prediction curves graphically. Moreover, a comparison with traditional Variational Iteration is also provided. It is concluded that the traditional method fails to converge for the updated models which involve the delayed differential equations. [ABSTRACT FROM AUTHOR]

In this paper, we have studied about the sensitivity analysis of the human immunodeficiency virus (HIV) protease inhibitor (PI) model and estimated the length of the delay. We have fabricated an HIV PI model accompanied with humoral immunity. Stability analysis of the constructed model about its steady states has been deliberated. We have evaluated some numerical simulations for PI model with humoral immunity by using the existing patient data. [ABSTRACT FROM AUTHOR]

Human immunodeficiency virus (HIV) is a lenti-virus (a member of the retrovirus family) that causes acquired immunodeficiency syndrome (AIDS), a critical condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections. Over the past few years HIV has been spreading rapidly in the population. Almost, everyday there are thousands of new human cases of HIV infection being recorded in the world and these occur in almost every country of the world. However, the spread of HIV is relatively faster in the developing countries as compared to developed countries because developing countries have limited resources. Worldwide, 70% of HIV infections in the adults have been transmitted through heterosexual contact and vertical transmission accounts for more than 90% of global infection in infants and children. In this paper, we propose a nonlinear mathematical model to study the spread of HIV by considering transmission of disease by heterosexual contact and vertical transmission. A stage structured model is proposed and analyzed by considering the total population variable and dividing the whole population under consideration into three stages: children, adults and old. Also, in this paper it is assumed that the rates of recruitment are different in different groups of population. Equilibria of the model and their stability are also discussed. Using the stability theory of differential equations and computer simulation, it is shown that due to the increase in the awareness of the disease in the adult class the total infective population decreases in the region under consideration. [ABSTRACT FROM AUTHOR]

In this paper, we study the application of a pulse vaccination strategy to eradicate hepatitis B and C modeled by SIV epidemic model. Since infection age is an important factor of hepatitis progression, we incorporate the infection age into the model. In this model, we consider the infectiousness of latent individuals. We derive the condition in which eradication solution is a global attractor, this condition depends on pulse vaccination proportion p and interpulse time T. We also obtain the condition of the global asymptotic stability of the solution. The condition shows that large enough pulse vaccination proportion and relatively small interpulse time lead to the eradication of hepatitis B and C. Moreover the results of the theoretical study might be instructive to the epidemiology of HIV. [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]

In this paper, we investigate the dynamics of a five-dimensional virus model incorporating saturation incidence rate, CTL immune response and three time delays which represent the latent period, virus production period and immune response delay, respectively. We begin this model by proving the positivity and boundedness of the solutions. Our model admits three possible equilibrium solutions, namely the infection-free equilibrium , the infectious equilibrium without immune response and the infectious equilibrium with immune response . Moreover, by analyzing corresponding characteristic equations, the local stability of each of the feasible equilibria and the existence of Hopf bifurcation at the equilibrium point are established, respectively. Further, by using fluctuation lemma and suitable Lyapunov functionals, it is shown that is globally asymptotically stable when the basic reproductive numbers for viral infection is less than unity. When the basic reproductive numbers for immune response is less than unity and is greater than unity, the equilibrium point is globally asymptotically stable. Finally, some numerical simulations are carried out for illustrating the theoretical results. [ABSTRACT FROM AUTHOR]

This paper studies some human immunodeficiency virus (HIV) models with switching parameters and pulse control. The classical virus dynamics model is first modified by incorporating switching parameters which are assumed to be time-varying. Some threshold conditions are derived to guarantee the virus elimination by utilizing a Razumikhin-type approach. The results show that the proper switching conditions chosen can increase the counts of CD4+ T-cells while reducing viral load. Pulse control strategies are then applied to the above model. More precisely, the treatment strategy and the vaccination strategy are applied to infected cells and uninfected cells, respectively. Each control strategy is analyzed to gauge its success in achieving viral suppression. Numerical simulations are performed to complement the analytical results and motivate future directions. [ABSTRACT FROM AUTHOR]

In this research paper, our main objective is to find out the meticulous role of activated dendritic cells (DCs) during the human immunodeficiency virus (HIV) infection process. DCs play a dual role by enhancing both HIV infection progression, as well as antiviral immune response. To explore the implications of these dual roles, we have formulated our mathematical model and analyzed the model by both analytical and numerical approaches. By using an impulsive differential equation, we have studied the effect of DC-based vaccination. Analytically we have determined the threshold value of drug dosage and dosing interval for optimum levels of infection. We have also investigated the effect of perfect adherence of drug dose on the immune cell count in extreme cases and observed that, systematic drug dose of the immune cells leads to its maximum level. [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]

In this paper, we propose a mathematical model for HIV-1 infection with three time delays. The model examines a viral-therapy for controlling infections by using an engineered virus to selectively eliminate infected cells. In our model, three time delays represent the latent period of pathogen virus, pathogen virus production period and recombinant (genetically modified) virus production period, respectively. Detailed theoretical analysis have demonstrated that the values of three delays can affect the stability of equilibrium solutions, can also lead to Hopf bifurcation and oscillated solutions of the system. Moreover, we give the conditions for the existence of stable positive equilibrium solution and Hopf bifurcation. Further, the properties of Hopf bifurcation are discussed. These theoretical results indicate that the delays play an important role in determining the dynamic behavior quantitatively. Therefore, it is a fact that delays are very important, which should not be missed in controlling HIV-1 infections. [ABSTRACT FROM AUTHOR]

In this paper, a nonlinear mathematical model is presented for the transmission dynamics of HIV/AIDS in Cuba. Due to Cuba's highly successful national prevention program, we assume that the only mode of transmission is through contact with those yet to be diagnosed with HIV. We find the equilibria of the governing nonlinear system, perform a linear stability analysis, and then provide results on global stability. [ABSTRACT FROM AUTHOR]

In this paper, the dynamics of mathematical model for infection of thymus gland by HIV-1 is analyzed by applying some perturbation through two different types of delays such as in terms of Hopf bifurcation analysis. Further, the conditions for the existence of Hopf bifurcation are derived by evaluating the characteristic equation. The direction of Hopf bifurcation and stability of bifurcating periodic solutions are determined by employing the center manifold theorem and normal form method. Finally, some of the numerical simulations are carried out to validate the derived theoretical results and main conclusions are included. [ABSTRACT FROM AUTHOR]

This paper presents a nonlinear sex-structured mathematical model to study the spread of HIV/AIDS by considering transmission of disease by heterosexual contact. The epidemic threshold and equilibria for the model are determined, local stability and global stability of both the "Disease-Free Equilibrium" (DFE) and "Endemic Equilibrium" (EE) are discussed in detail. The DFE is shown to be locally and globally stable when the basic reproductive number ℛ0 is less than unity. We also prove that the EE is locally and globally asymptotically stable under some conditions. Finally, numerical simulations are reported to support the analytical findings. [ABSTRACT FROM AUTHOR]

Mathematical modeling plays a crucial role in understanding the dynamics of Human immunodeficiency virus (HIV) disease. Most models deal with the vertical and horizontal spread of disease, but few studies have focused on the evolutionary dynamics of HIV at the cellular level. In this paper, we present an HIV model to analyze the dynamics of HIV infection at the cellular level to produce more natural results. We present a detailed stability analysis of disease-free and viral-persistence equilibrium in the system. In addition, sensitivity analysis and optimal control strategies are used to analyze the role of antiretroviral drug therapy and dietary supplements in controlling the concentration of infected cells and viruses. [ABSTRACT FROM AUTHOR]

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]

In this paper, a mathematical model for the effect of drug therapy on the in-host dynamics of HIV is considered and analyzed. As the process of reverse transcription is highly error prone, it causes mutation of virus which results in the emergence of drug resistant virus. This is also accounted in the model and corresponding model with both drug resistant and drug sensitive viral strains is studied. We found that, if reproductive ratios for both the strains are less than one, the virus population goes to extinction. If the reproductive ratio of either strain is greater than one and the reproductive ratio of drug resistant virus is smaller than that of drug sensitive virus then both the virus strains persist and infection is not cleared. However if reproductive ratio of drug resistant virus is greater than that of drug sensitive virus then the drug resistant virus out-competes the drug sensitive virus and only drug resistant virus survives. Hence the ratio of two reproduction ratios works as invading capacity threshold value for drug resistant strain. We also noted that by increasing the effective efficacy of the drug, virus may be cleared. Numerical simulations are performed to support and elaborate the analytical findings. [ABSTRACT FROM AUTHOR]

The objective of this paper is to study the global dynamics of a simple SI model with two explicit age groups and apply the findings to the HIV dynamics in the United States. Specifically, we would like to explore the long term HIV dynamics to answer questions such as what will happen to human population level if all the demographical and epidemiological parameters stay constant. We also wonder if treatment alone will actually slow the spread of HIV or not. We divide the population into juvenile and adult groups. Only adults are assumed to be sexually active and we implicitly assume that the sex ratio is constant. We also assume that infected adults may produce both susceptible newborns and infected newborns. The model is fit with parameters from the HIV epidemic in the US. It produces an optimistic outcome: if nothing changes, the USA infected population may be halved in about 20 years. However, if treatment is found to extend the life expectance of infected individuals to 30 years or more, then the number of infected adults may actually increase in the next 20 years or so. This creates a dilemma: to treat or not to treat? [ABSTRACT FROM AUTHOR]

This paper presents a new neural learning algorithm for protease cleavage site prediction. The basic idea is to replace the radial basis function used in radial basis function neural networks by a so-called bio-basis function using amino acid similarity matrices. Mutual information is used to select bio-bases and a corresponding selection algorithm is developed. The algorithm has been applied to the prediction of HIV and Hepatitis C virus protease cleavage sites in proteins with success. [ABSTRACT FROM AUTHOR]

Both the International Labor Organization (ILO) and the World Health Organization (WHO) concur that occupational health and safety in Africa needs strengthening. In support of this realization are the need to maintain and promote workers' health and working capacity, and the need to become conducive to safety and health by improving both the working environment and work. The fight against HIV and AIDS in the workplace is a continental priority. In the absence of any other definitive or similar study, this study aims to establish a valid baseline assessment of the levels of knowledge, types of attitudes, perceptions and beliefs of construction workers in South Africa regarding HIV infection and AIDS. It performs both a descriptive function with respect to how many workers have correct knowledge regarding AIDS and HIV and a predictive function in terms of how knowledge, attitudes, perceptions, beliefs, behaviors and certain biographical traits relate to one another. This paper examines the attitudes and perceptions of HIV and AIDS among construction workers as determined during the first phase of an exploratory study commenced in August 2002. [ABSTRACT FROM AUTHOR]

We present a review and comparison of several recent differential equations models of treatment of HIV-1 infection. We seek to clarify the role of the natural anti-HIV immune response and determine its effect upon optimal treatment schemes. In this paper, we consider systems in which treatment is expressed as a forcing function, as well as those in which we determine optimal treatment via control theoretic techniques. The primary goal of this study is to compare treatment schemes for systems in which a natural nonconstant immune response of the patient is considered explicitly with those that consider implicitly a constant non-specific immune response. We find that when the natural immune response can be boosted sufficiently, drug levels may not need to be as high as previously supposed. This implies that a treatment scenario in which intervals of drug treatment are alternated with some form of immune-boosting therapy may be highly beneficial in terms of reducing toxicity to the patient. Additionally, in developing countries where HIV infection is widespread and sufficient funds are not available to supply rigourous drug regimens, the implications of these models are profound, as they suggest methods of treating HIV at a minimal cost. [ABSTRACT FROM AUTHOR]

In this paper, neglecting the effects of free virus, we consider a simple model of cell-to-cell spread of HIV-1. We discuss the impact of the CD8+ cell non-cytotoxic anti-viral response (CNAR) and cytotoxic T lymphocyte (CTL) activity on infection by HIV-1. Two types of models are considered: the ordinary differential equation (ODE) model and the discrete time delay differential equation (DDE) system. The steady states of the ODE model are globally asymptotically stable respectively under two threshold criteria. In the DDE model, the global stability of the infected steady state of the ODE model becomes only ultimately stable. Moreover, at a certain interval of the time delay, the DDE model will produce Hopf bifurcation or periodic solutions. The introduction of CTL and CNAR will change the values of these steady states and induce fluctuations in the cell concentration. It also affects the critical value of the time delay and is of utility in the interpretation of typical HIV-dynamics data resulting from clinical trials. The DDE model produces sustained infective oscillations in some real parameter values, which is different from the result of the similar cell-free viral spread model with delay. [ABSTRACT FROM AUTHOR]

HIV mutations occur frequently despite the substantial success of combination antiretroviral therapy, which significantly impairs HIV progression. Failure to develop specific vaccines, the occurrence of drug-resistant strains, and the high incidence of adverse effects due to combination antiviral therapy regimens call for novel and safer antivirals. Natural products are an important source of new anti-infective agents. For instance, curcumin inhibits HIV and inflammation in cell culture assays. Curcumin, the principal constituent of the dried rhizomes of Curcuma longa L. (turmeric), is known as a strong anti-oxidant and anti-inflammatory agent with different pharmacological effects. This work aims to assess curcumin's inhibitory effects on HIV in vitro and to explore the underpinning mechanism, focusing on CCR5 and the transcription factor forkhead box protein P3 (FOXP3). First, curcumin and the RT inhibitor zidovudine (AZT) were evaluated for their inhibitory properties. HIV-1 pseudovirus infectivity was determined by green fluorescence and luciferase activity measurements in HEK293T cells. AZT was used as a positive control that inhibited HIV-1 pseudoviruses dose-dependently, with IC50 values in the nanomolar range. Then, a molecular docking analysis was carried out to assess the binding affinities of curcumin for CCR5 and HIV-1 RNase H/RT. The anti-HIV activity assay showed that curcumin inhibited HIV-1 infection, and the molecular docking analysis revealed equilibrium dissociation constants of − 9.8 kcal/mol and − 9.3 kcal/mol between curcumin and CCR5 and HIV-1 RNase H/RT, respectively. To examine curcumin's anti-HIV effect and its mechanism in vitro, cell cytotoxicity, transcriptome sequencing, and CCR5 and FOXP3 amounts were assessed at different concentrations of curcumin. In addition, human CCR5 promoter deletion constructs and the FOXP3 expression plasmid pRP–FOXP3 (with an EGFP tag) were generated. Whether FOXP3 DNA binding to the CCR5 promoter was blunted by curcumin was examined using transfection assays employing truncated CCR5 gene promoter constructs, a luciferase reporter assay, and a chromatin immunoprecipitation (ChIP) assay. Furthermore, micromolar concentrations of curcumin inactivated the nuclear transcription factor FOXP3, which resulted in decreased expression of CCR5 in Jurkat cells. Moreover, curcumin inhibited PI3K-AKT activation and its downstream target FOXP3. These findings provide mechanistic evidence encouraging further assessment of curcumin as a dietary agent used to reduce the virulence of CCR5-tropic HIV-1. Curcumin-mediated FOXP3 degradation was also reflected in its functions, namely, CCR5 promoter transactivation and HIV-1 virion production. Furthermore, curcumin inhibition of CCR5 and HIV-1 might constitute a potential therapeutic strategy for reducing HIV progression. [ABSTRACT FROM AUTHOR]

A model for assessing the impact of key population at risk in spreading HIV/ AIDS is designed. The model is shown to have a globally asymptotically stable (GAS) disease-free equilibrium whenever the associated reproduction number is less than unity. It has a unique GAS endemic equilibrium whenever reproduction number exceeds unity, if there is no back and forth movement in susceptible classes. It is shown that if infected individuals with high risk abandon their risky behavioral practices, then the disease burden will reduce. Furthermore, if infected individuals with low risk do not adopt risky behaviors then the transmission of the disease will decrease. Partial Rank Correlation Coefficient (PRCC) indices are assessed using all the infection-related classes and basic reproduction number of the model. Uncertainty and sensitivity analysis results show that controlling the effective contact rate, disease-induced death rate in AIDS stage with low and high risk classes will help controlling the transmission of the disease. [ABSTRACT FROM AUTHOR]