# American Institute of Mathematical Sciences

ISSN:
1551-0018

eISSN:
1547-1063

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## Mathematical Biosciences & Engineering

2015 , Volume 12 , Issue 3

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2015, 12(3): 415-429 doi: 10.3934/mbe.2015.12.415 +[Abstract](1587) +[PDF](481.0KB)
Abstract:
We propose and study a model for sexually transmitted infections on uncorrelated networks, where both differential susceptibility and infectivity are considered. We first establish the spreading threshold, which exists even in the infinite networks. Moreover, it is possible to have backward bifurcation. Then for bounded hard-cutoff networks, the stability of the disease-free equilibrium and the permanence of infection are analyzed. Finally, the effects of two immunization strategies are compared. It turns out that, generally, the targeted immunization is better than the proportional immunization.
2015, 12(3): 431-449 doi: 10.3934/mbe.2015.12.431 +[Abstract](2333) +[PDF](7039.4KB)
Abstract:
In this paper, we include two time delays in a mathematical model for the CD8$^+$ cytotoxic T lymphocytes (CTLs) response to the Human T-cell leukaemia virus type I (HTLV-I) infection, where one is the intracellular infection delay and the other is the immune delay to account for a series of immunological events leading to the CTL response. We show that the global dynamics of the model system are determined by two threshold values $R_0$, the corresponding reproductive number of a viral infection, and $R_1$, the corresponding reproductive number of a CTL response, respectively. If $R_0<1$, the infection-free equilibrium is globally asymptotically stable, and the HTLV-I viruses are cleared. If $R_1 < 1 < R_0$, the immune-free equilibrium is globally asymptotically stable, and the HTLV-I infection is chronic but with no persistent CTL response. If $1 < R_1$, a unique HAM/TSP equilibrium exists, and the HTLV-I infection becomes chronic with a persistent CTL response. Moreover, we show that the immune delay can destabilize the HAM/TSP equilibrium, leading to Hopf bifurcations. Our numerical simulations suggest that if $1 < R_1$, an increase of the intracellular delay may stabilize the HAM/TSP equilibrium while the immune delay can destabilize it. If both delays increase, the stability of the HAM/TSP equilibrium may generate rich dynamics combining the stabilizing" effects from the intracellular delay with those destabilizing" influences from immune delay.
2015, 12(3): 451-472 doi: 10.3934/mbe.2015.12.451 +[Abstract](1621) +[PDF](3357.8KB)
Abstract:
Two hyperbolic reaction-diffusion models are built up in the framework of Extended Thermodynamics in order to describe the spatio-temporal interactions occurring in a two or three compartments aquatic food chain. The first model focuses on the dynamics between phytoplankton and zooplankton, whereas the second one accounts also for the nutrient. In these models, infections and influence of illumination on photosynthesis are neglected. It is assumed that the zooplankton predation follows a Holling type-III functional response, while the zooplankton mortality is linear. Owing to the hyperbolic structure of our equations, the wave processes occur at finite velocity, so that the paradox of instantaneous diffusion of biological quantities, typical of parabolic systems, is consequently removed. The character of steady states and travelling waves, together with the occurrence of Hopf bifurcations, is then discussed through linear stability analysis. The governing equations are also integrated numerically to validate the analytical results herein obtained and to extract additional information on the population dynamics.
2015, 12(3): 473-490 doi: 10.3934/mbe.2015.12.473 +[Abstract](1733) +[PDF](607.8KB)
Abstract:
Botanical epidemic models are very important tools to study invasion, persistence and control of diseases. It is well known that limitations arise from considering constant infection rates. We replace this hypothesis in the framework of delay differential equations by proposing a delayed epidemic model for plant--pathogen interactions with host demography. Sufficient conditions for the global stability of the pathogen-free equilibrium and the permanence of the system are among the results obtained through qualitative analysis. We also show that the delay can cause stability switches of the coexistence equilibrium. In the undelayed case, we prove that the onset of oscillations may occur through Hopf bifurcation.
2015, 12(3): 491-501 doi: 10.3934/mbe.2015.12.491 +[Abstract](1982) +[PDF](384.6KB)
Abstract:
We present a model that describes the growth, division and death of a cell population structured by size. The model is an extension of that studied by Hall and Wake (1989) and incorporates the asymmetric division of cells. We consider the case of binary asymmetrical splitting in which a cell of size $\xi$ divides into two daughter cells of different sizes and find the steady size distribution (SSD) solution to the non-local differential equation. We then discuss the shape of the SSD solution. The existence of higher eigenfunctions is also discussed.
2015, 12(3): 503-523 doi: 10.3934/mbe.2015.12.503 +[Abstract](1836) +[PDF](694.5KB)
Abstract:
Symmetric evolutionary games, i.e., evolutionary games with symmetric fitness matrices, have important applications in population genetics, where they can be used to model for example the selection and evolution of the genotypes of a given population. In this paper, we review the theory for obtaining optimal and stable strategies for symmetric evolutionary games, and provide some new proofs and computational methods. In particular, we review the relationship between the symmetric evolutionary game and the generalized knapsack problem, and discuss the first and second order necessary and sufficient conditions that can be derived from this relationship for testing the optimality and stability of the strategies. Some of the conditions are given in different forms from those in previous work and can be verified more efficiently. We also derive more efficient computational methods for the evaluation of the conditions than conventional approaches. We demonstrate how these conditions can be applied to justifying the strategies and their stabilities for a special class of genetic selection games including some in the study of genetic disorders.
2015, 12(3): 525-536 doi: 10.3934/mbe.2015.12.525 +[Abstract](2349) +[PDF](441.0KB)
Abstract:
In this paper, the dynamical behavior of a viral infection model with general incidence rate and two time delays is studied. By using the Lyapunov functional and LaSalle invariance principle, the global stabilities of the infection-free equilibrium and the endemic equilibrium are obtained. We obtain a threshold of the global stability for the uninfected equilibrium, which means the disease will be under control eventually. These results can be applied to a variety of viral infections of disease that would make it possible to devise optimal treatment strategies. Numerical simulations with application to HIV infection are given to verify the analytical results.
2015, 12(3): 537-554 doi: 10.3934/mbe.2015.12.537 +[Abstract](1503) +[PDF](504.5KB)
Abstract:
In this paper, we focus on the behaviour of periodic solutions to a cell-scale electropermeabilization model previously proposed by Kavian et al. [6]. Since clinical permeabilization protocols mostly submit cancer cells to trains of periodic pulses, we investigate on parameters that modify significantly the resulting permeabilization. Theoretical results of existence and uniqueness of periodic solutions are presented, for two different models of membrane electric conductivity. Numerical simulations were performed to corroborate these results and illustrate the asymptotic convergence to periodic solutions, as well as the dependency on biological parameters such as the cell size and the extracellular conductivity.
2015, 12(3): 555-564 doi: 10.3934/mbe.2015.12.555 +[Abstract](1880) +[PDF](396.2KB)
Abstract:
Threshold dynamics of epidemic models in periodic environments attract more attention. But there are few papers which are concerned with the case where the infected compartments satisfy a delay differential equation. For this reason, we investigate the dynamical behavior of a periodic SIR model with delay in an infected compartment. We first introduce the basic reproduction number $\mathcal {R}_0$ for the model, and then show that it can act as a threshold parameter that determines the uniform persistence or extinction of the disease. Numerical simulations are performed to confirm the analytical results and illustrate the dependence of $\mathcal {R}_0$ on the seasonality and the latent period.
2015, 12(3): 565-584 doi: 10.3934/mbe.2015.12.565 +[Abstract](2571) +[PDF](549.6KB)
Abstract:
The basic reproduction number of deterministic models is an essential quantity to predict whether an epidemic will spread or not. Thresholds for disease extinction contribute crucial knowledge of disease control, elimination, and mitigation of infectious diseases. Relationships between basic reproduction numbers of two deterministic network-based ordinary differential equation vector-host models, and extinction thresholds of corresponding stochastic continuous-time Markov chain models are derived under some assumptions. Numerical simulation results for malaria and Rift Valley fever transmission on heterogeneous networks are in agreement with analytical results without any assumptions, reinforcing that the relationships may always exist and proposing a mathematical problem for proving existence of the relationships in general. Moreover, numerical simulations show that the basic reproduction number does not monotonically increase or decrease with the extinction threshold. Consistent trends of extinction probability observed through numerical simulations provide novel insights into mitigation strategies to increase the disease extinction probability. Research findings may improve understandings of thresholds for disease persistence in order to control vector-borne diseases.
2015, 12(3): 585-607 doi: 10.3934/mbe.2015.12.585 +[Abstract](1664) +[PDF](1983.6KB)
Abstract:
In this paper, we discuss methods for developing a stochastic model which incorporates behavior differences in the predation movements of Anelosimus studiosus (a subsocial spider). Stochastic models for animal movement and, in particular, spider predation movement have been developed previously; however, this paper focuses on the development and implementation of the necessary mathematical and statistical methods required to expand such a model in order to capture a variety of distinct behaviors. A least squares optimization algorithm is used for parameter estimation to fit a single stochastic model to an individual spider during predation resulting in unique parameter values for each spider. Similarities and variations between parameter values across the spiders are analyzed and used to estimate probability distributions for the variable parameter values. An aggregate stochastic model is then created which incorporates the individual dynamics. The comparison between the optimal individual models to the aggregate model indicate the methodology and algorithm developed in this paper are appropriate for simulating a range of individualistic behaviors.
2015, 12(3): 609-623 doi: 10.3934/mbe.2015.12.609 +[Abstract](2456) +[PDF](513.6KB)
Abstract:
Launching a prevention campaign to contain the spread of infection requires substantial financial investments; therefore, a trade-off exists between suppressing the epidemic and containing costs. Information exchange among individuals can occur as physical contacts (e.g., word of mouth, gatherings), which provide inherent possibilities of disease transmission, and non-physical contacts (e.g., email, social networks), through which information can be transmitted but the infection cannot be transmitted. Contact network (CN) incorporates physical contacts, and the information dissemination network (IDN) represents non-physical contacts, thereby generating a multilayer network structure. Inherent differences between these two layers cause alerting through CN to be more effective but more expensive than IDN. The constraint for an epidemic to die out derived from a nonlinear Perron-Frobenius problem that was transformed into a semi-definite matrix inequality and served as a constraint for a convex optimization problem. This method guarantees a dying-out epidemic by choosing the best nodes for adopting preventive behaviors with minimum monetary resources. Various numerical simulations with network models and a real-world social network validate our method.
2015, 12(3): 625-642 doi: 10.3934/mbe.2015.12.625 +[Abstract](2365) +[PDF](587.9KB)
Abstract:
Granulomas play a centric role in tuberculosis (TB) infection progression. Multiple granulomas usually develop within a single host. These granulomas are not synchronized in size or bacteria load, and will follow different trajectories over time. How the fate of individual granulomas influence overall infection outcome at host scale is not understood, although computational models have been developed to predict single granuloma behavior. Here we present a within-host population model that tracks granulomas in two key organs during Mycobacteria tuberculosis (Mtb) infection: lung and lymph nodes (LN). We capture various time courses of TB progression, including latency and reactivation. The model predicts that there is no steady state; rather it is a continuous process of progressing to active disease over differing time periods. This is consistent with recently posed ideas suggesting that latent TB exists as a spectrum of states and not a single state. The model also predicts a dual role for granuloma development in LNs during Mtb infection: in early phases of infection granulomas suppress infection by providing additional antigens to the site of immune priming; however, this induces a more rapid reactivation at later stages by disrupting immune responses. We identify mechanisms that strongly correlate with better host-level outcomes, including elimination of uncontained lung granulomas by inducing low levels of lung tissue damage and inhibition of bacteria dissemination within the lung.

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