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In this paper, a compartmental model on the co-infection of pneumonia and HIV/AIDS with optimal control strategies was formulated using the system of ordinary differential equations. Using qualitative methods, we have analysed the mono-infection and HIV/AIDS and pneumonia co-infection models. We have computed effective reproduction numbers by applying the next-generation matrix method, applying Castillo Chavez criteria the models disease-free equilibrium points global stabilities were shown, while we have used the Centre manifold criteria to determine that the pneumonia infection and pneumonia and HIV/AIDS co-infection exhibit the phenomenon of backward bifurcation whenever the corresponding effective reproduction number is less than unity. We carried out the numerical simulations to investigate the behaviour of the co-infection model solutions. Furthermore,wehave investigated various optimal control strategies to predict the best control strategy to minimize and possibly to eradicate the HIV/AIDS and pneumonia co-infection from the community. [ABSTRACT FROM AUTHOR]

Latently infected CD 4 + T cells represent one of the major obstacles to HIV eradication even after receiving prolonged highly active anti-retroviral therapy (HAART). Long-term use of HAART causes the emergence of drug-resistant virus which is then involved in HIV transmission. In this paper, we develop mathematical HIV models with staged disease progression by incorporating entry inhibitor and latently infected cells. We find that entry inhibitor has the same effect as protease inhibitor on the model dynamics and therefore would benefit HIV patients who developed resistance to many of current anti-HIV medications. Numerical simulations illustrate the theoretical results and show that the virus and latently infected cells reach an infected steady state in the absence of treatment and are eliminated under treatment whereas the model including homeostatic proliferation of latently infected cells maintains the virus at low level during suppressive treatment. Therefore, complete cure of HIV needs complete eradication of latent reservoirs. [ABSTRACT FROM AUTHOR]

HIV is a virus that weakens a person's immune system. HIV has three stages, and AIDS is the most severe stage of HIV (Stage 3). People with HIV should take medicine (called ART) recommended by WHO as soon as possible to reduce the amount of virus in the body. In this paper, we formulate a mathematical model for HIV/AIDS with a new approach by focusing on two groups of infectious individuals, HIV and AIDS. We also introduce a controlled class (treated patients and being monitored), and people in this class can spread the disease. We further investigate the essential dynamics of the model through an equilibrium analysis. Optimal control theory is applied to explore effective treatment strategies by combining two control measures: standard antiretroviral therapy and AIDS treatments. Numerical simulation results show the effects of the two time-dependent controls, and they can be used as guidelines for public health interventions. [ABSTRACT FROM AUTHOR]

This paper aims to analyse stability and Hopf bifurcation of the HIV-1 model with immune delay under the functional response of the Holling II type. The global stability analysis has been considered by Lyapunov–LaSalle theorem. And stability and the sufficient condition for the existence of Hopf Bifurcation of the infected equilibrium of the HIV-1 model with immune response are also studied. Some numerical simulations verify the above results. Finally, we propose a novel three dimension system to the future study. [ABSTRACT FROM AUTHOR]

In this paper, a delayed human immunodeficiency virus (HIV) model with apoptosis of cells has been studied. Both immunological and intracellular delay have been incorporated to make the model more relevant. Firstly, the model has been investigated using local stability analysis. Next, the global stability analysis of steady states has been performed. The stability switch criteria taking the delay as the bifurcating parameter, leading to Hopf bifurcation has been studied. The transition of the system from order to chaos has been explored, and the analytical results have been verified by numerical simulations. The results thus can be used to describe the extensive dynamics exhibited by the model introduced in this article. The effects of apoptosis on viral load has been studied in the model numerically. [ABSTRACT FROM AUTHOR]

In this paper, with eclipse stage in consideration, we propose an HIV-1 infection model with a general incidence rate and CTL immune response. We first study the existence and local stability of equilibria, which is characterized by the basic infection reproduction number R 0 and the basic immunity reproduction number R 1 . The local stability analysis indicates the occurrence of transcritical bifurcations of equilibria. We confirm the bifurcations at the disease-free equilibrium and the infected immune-free equilibrium with transmission rate and the decay rate of CTLs as bifurcation parameters, respectively. Then we apply the approach of Lyapunov functions to establish the global stability of the equilibria, which is determined by the two basic reproduction numbers. These theoretical results are supported with numerical simulations. Moreover, we also identify the high sensitivity parameters by carrying out the sensitivity analysis of the two basic reproduction numbers to the model parameters. [ABSTRACT FROM AUTHOR]

In this paper, we formulate a stochastic model for hepatitis B virus transmission with the effect of fluctuation environment. We divide the total population into four different compartments, namely, the susceptible individuals in which the disease transmission rate is distributed by white noise, the acutely infected individuals in which the same perturbation occur, the chronically infected individuals and the recovered individuals. We use the stochastic Lyapunov function theory to construct a suitable stochastic Lyapunov function for the existence of positive solution. We also then establish the sufficient conditions for the hepatitis B extinction and the hepatitis B persistence. At the end numerical simulation is carried out by using the stochastic Runge–Kutta method to support our analytical findings. [ABSTRACT FROM AUTHOR]

In this study, we apply optimal control theory to an immunoepidemiological model of HIV and opioid epidemics. For the multiscale model, we used four controls: treating the opioid use, reducing HIV risk behaviour among opioid users, entry inhibiting antiviral therapy, and antiviral therapy which blocks the viral production. Two population-level controls are combined with two within-host-level controls. We prove the existence and uniqueness of an optimal control quadruple. Comparing the two population-level controls,wefind that reducing the HIV risk of opioid users has a stronger impact on the population who is both HIV-infected and opioid-dependent than treating the opioid disorder. The within-host-level antiviral treatment has an effect not only on the co-affected population but also on the HIV-only infected population. Our findings suggest that the most effective strategy for managing the HIV and opioid epidemics is combining all controls at both within-host and between-host scales. [ABSTRACT FROM AUTHOR]

HIV can infect cells via virus-to-cell infection or cell-to-cell viral transmission. These two infection modes may occur in a synergistic way and facilitate viral spread within an infected individual. In this paper, we developed an HIV latent infection model including both modes of transmission and time delays between viral entry and integration or viral production. We analysed the model by defining the basic reproductive number, showing the existence, positivity and boundedness of the solution, and proving the local and global stability of the infection-free and infected steady states. Numerical simulations have been performed to illustrate the theoretical results and evaluate the effects of time delays and fractions of infection leading to latency on the virus dynamics. The estimates of the relative contributions to the HIV latent reservoir and the virus population from the two modes of transmission have also been provided. [ABSTRACT FROM PUBLISHER]

This paper investigates consequences of vaccine implementation strategies for infectious diseases by a mathematical model. For an infectious disease, the degree of infection may vary widely among the individuals. Reports show that individuals belonging to certain groups possess considerably higher risk to infection. Incorporating this phenomenon into vaccination strategies, the host is categorized into different groups to measure the outcome of the vaccination. A mathematical model is proposed and analysed to evaluate this measure. Our results suggest that vaccinating a group with certain priority may lead to elimination of the disease effectively. The strategy is cost-effective as well. [ABSTRACT FROM AUTHOR]

HIV continues to be a major global health issue, having claimed millions of lives in the last few decades. While several empirical studies support the fact that proper nutrition is useful in the fight against HIV, very few studies have focused on developing and using mathematical modelling approaches to assess the association between HIV, human immune response to the disease, and nutrition. We develop a within-host model for HIV that captures the dynamic interactions between HIV, the immune system and nutrition. We find that increased viral activity leads to increased serum protein levels. We also show that the viral production rate is positively correlated with HIV viral loads, as is the enhancement rate of protein by virus. Although our numerical simulations indicate a direct correlation between dietary protein intake and serum protein levels in HIV-infected individuals, further modelling and clinical studies are necessary to gain comprehensive understanding of the relationship. [ABSTRACT FROM AUTHOR]

A multi-patch HIV/AIDS model with heterosexual transmission is formulated to investigate the impact of population migration on the spread of HIV/AIDS. We derive the basic reproduction number $ R_{0} $ R 0 and prove that if $ R_{0} \lt 1 $ R 0 < 1 , the disease-free equilibrium is globally asymptotically stable. If $ R_{0} \gt 1 $ R 0 > 1 and certain conditions are satisfied, the endemic equilibrium is globally asymptotically stable. We apply the model to two patches and conduct numerical simulations. If HIV/AIDS becomes extinct in each patch when two patches are isolated, the disease remains extinct in two patches when the population migration occurs; if HIV/AIDS spreads in each patch when two patches are isolated, the disease remains persistent in two patches when the population migration occurs; if the disease disappears in one patch and spreads in the other patch when they are isolated, the disease can spread or disappear in two patches if migration rates of individuals are suitably chosen. [ABSTRACT FROM AUTHOR]

In this paper, a two-strain model that links immunological and epidemiological dynamics across scales is formulated. On the within-host scale, the two strains eliminate each other with the strain with the larger immunological reproduction persisting. However, on the population scale superinfection is possible, with the strain with larger immunological reproduction number super-infecting the strain with the smaller immunological reproduction number. The two models are linked through the age-since-infection structure of the epidemiological variables. In addition, the between-host transmission and the disease-induced death rate depend on the within-host viral load. The immunological reproduction numbers, the epidemiological reproduction numbers and invasion reproduction numbers are computed. Besides the disease-free equilibrium, there are two population-level strain one and strain two isolated equilibria, as well as a population-level coexistence equilibrium when both invasion reproduction numbers are greater than one. The single-strain population-level equilibria are locally asymptotically stable suggesting that in the absence of superinfection oscillations do not occur, a result contrasting previous studies of HIV age-since-infection structured models. Simulations suggest that the epidemiological reproduction number and HIV population prevalence are monotone functions of the within-host parameters with reciprocal trends. In particular, HIV medications that decrease within-host viral load also increase overall population prevalence. The effect of the immunological parameters on the population reproduction number and prevalence is more pronounced when the initial viral load is lower. [ABSTRACT FROM AUTHOR]

One major drawback associated with the use of anti-retroviral drugs in curtailing HIV spread in a population is the emergence and transmission of HIV strains that are resistant to these drugs. This paper presents a deterministic HIV treatment model, which incorporates a wild (drug sensitive) and a drug-resistant strain, for gaining insights into the dynamical features of the two strains, and determining effective ways to control HIV spread under this situation. Rigorous qualitative analysis of the model reveals that it has a globally asymptotically stable disease-free equilibrium whenever a certain epidemiological threshold (R t 0) is less than unity and that the disease will persist in the population when this threshold exceeds unity. Further, for the case where R t 0 > 1, it is shown that the model can have two co-existing endemic equilibria, and competitive exclusion phenomenon occurs whenever the associated reproduction number of the resistant strain (R t r) is greater than that of the wild strain (R t w). Unlike in the treatment model, it is shown that the model without treatment can have a family of infinitely many endemic equilibria when its associated epidemiological threshold (R(0)) exceeds unity. For the case when [Formula in text], it is shown that the widespread use of treatment against the wild strain can lead to its elimination from the community if the associated reduction in infectiousness of infected individuals (treated for the wild strain) does not exceed a certain threshold value (in this case, the use of treatment is expected to make R t w < R t r.

In this paper, we rigorously analyse an ordinary differential equation system that models fighting the HIV-1 virus with a genetically modified virus. We show that when the basic reproduction ratio R0<1, then the infection-free equilibrium E0 is globally asymptotically stable; when R0>1, E0 loses its stability and there is the single-infection equilibrium Es. If R0∈(1, 1+δ) where δ is a positive constant explicitly depending on system parameters, then the single-infection equilibrium Es that is globally asymptotically stable, while when R0>1+δ, Es becomes unstable and the double-infection equilibrium Ed comes into existence. When R0 is slightly larger than 1+δ, Ed is stable and it loses its stability via Hopf bifurcation when R0 is further increased in some ways. Through a numerical example and by applying a normal form theory, we demonstrate how to determine the bifurcation direction and stability, as well as the estimates of the amplitudes and the periods of the bifurcated periodic solutions. We also perform numerical simulations which agree with the theoretical results. The approaches we use here are a combination of analysis of characteristic equations, fluctuation lemma, Lyapunov function and normal form theory. [ABSTRACT FROM AUTHOR]

This paper is devoted to the presentation and study of a specific stochastic epidemic model accounting for the effect of contact-tracing on the spread of an infectious disease. Precisely, one considers here the situation in which individuals identified as infected by the public health detection system may contribute to detecting other infectious individuals by providing information related to persons with whom they have had possibly infectious contacts. The control strategy, which consists of examining each individual who has been able to be identified on the basis of the information collected within a certain time period, is expected to efficiently reinforce the standard random-screening-based detection and considerably ease the epidemic. In the novel modelling of the spread of a communicable infectious disease considered here, the population of interest evolves through demographic, infection and detection processes, in a way that its temporal evolution is described by a stochastic Markov process, of which the component accounting for the contact-tracing feature is assumed to be valued in a space of point measures. For adequate scalings of the demographic, infection and detection rates, it is shown to converge to the weak deterministic solution of a PDE system, as a parameter n, interpreted as the population size, roughly speaking, becomes larger. From the perspective of the analysis of infectious disease data, this approximation result may serve as a key tool for exploring the asymptotic properties of standard inference methods such as maximum likelihood estimation. We state preliminary statistical results in this context. Eventually, relations of the model with the available data of the HIV epidemic in Cuba, in which country a contact-tracing detection system has been set up since 1986, is investigated and numerical applications are carried out. [ABSTRACT FROM AUTHOR]

In this paper, a delayed human immunodeficiency virus (HIV) model with apoptosis of cells has been studied. Both immunological and intracellular delay have been incorporated to make the model more relevant. Firstly, the model has been investigated using local stability analysis. Next, the global stability analysis of steady states has been performed. The stability switch criteria taking the delay as the bifurcating parameter, leading to Hopf bifurcation has been studied. The transition of the system from order to chaos has been explored, and the analytical results have been verified by numerical simulations. The results thus can be used to describe the extensive dynamics exhibited by the model introduced in this article. The effects of apoptosis on viral load has been studied in the model numerically.

The problem of who is mixing with whom is of great theoretical importance in the context of heterosexual mixing. In this article, we publish for the first time, data from a study carried out in 1989 that had the goal of estimating who is mixing with whom, in heterosexually active college populations in the presence of co-factors like drinking. The gathering of these data and the challenges involved in modelling the interaction between and among heterosexually active populations of individuals are highlighted in this manuscript. The modelling is based on the assumptions that at least two processes are involved: individual affinities or preferences determine 'what we want' while mixing patterns describe 'what we get'. We revisit past results on the role of affinity/preference on observed mixing patterns in one- and two-sex mixing populations. Some new results for homosexually active populations are presented. The study of mixing is but the means to an end and consequently, we also look at the role of affinity on epidemics as filtered by observed mixing patterns. It would not be surprising to observe that highly distinct preference or mixing structures may actually lead to quite similar epidemic patterns. [ABSTRACT FROM AUTHOR]

A system of ordinary differential equations is formulated to describe the pathogenesis of HIV infection, wherein certain features that have been shown to be important by recent experimental research are incorporated in the model. These include the role of CD4+memory cells that serve as a major reservoir of latently infected cells, a critical role for T-helper cells in the generation of CD8 memory cells capable of efficient recall response, and stimulation by antigens other than HIV. A stability analysis illustrates the capability of this model in admitting multiple locally asymptotically stable (locally a.s.) off-treatment equilibria. We show that this more biologically detailed model can exhibit the phenomenon of transient viremia experienced by some patients on therapy with viral load levels suppressed below the detection limit. We also show that the loss of CD4+T-cell help in the generation of CD8+memory cells leads to larger peak values for the viral load during transient viremia. Censored clinical data is used to obtain parameter estimates. We demonstrate that using a reduced set of 16 free parameters, obtained by fixing some parameters at their population averages, the model provides reasonable fits to the patient data and, moreover, that it exhibits good predictive capability. We further show that parameter values obtained for most clinical patients do not admit multiple locally a.s off-treatment equilibria. This suggests that treatment to move from a high viral load equilibrium state to an equilibrium state with a lower (or zero) viral load is not possible for these patients. [ABSTRACT FROM AUTHOR]