Journal of Biological Dynamics最新文献

This paper is concerned with a stochastic predator-prey model with Holling II increasing function in the predator. By applying the Lyapunov analysis method, we demonstrate the existence and uniqueness of the global positive solution. Then we show there is a stationary distribution which implies the stochastic persistence of the predator and prey in the model. Moreover, we obtain respectively sufficient conditions for weak persistence in the mean and extinction of the prey and extinction of the predator. Finally, some numerical simulations are given to illustrate our main results and the discussion and conclusion are presented.

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.

In this paper, we introduce three within-host and one within-vector models of Zika virus. The within-host models are the target cell limited model, the target cell limited model with natural killer (NK) cells class, and a within-host-within-fetus model of a pregnant individual. The within-vector model includes the Zika virus dynamics in the midgut and salivary glands. The within-host models are not structurally identifiable with respect to data on viral load and NK cell counts. After rescaling, the scaled within-host models are locally structurally identifiable. The within-vector model is structurally identifiable with respect to viremia data in the midgut and salivary glands. Using Monte Carlo Simulations, we find that target cell limited model is practically identifiable from data on viremia; the target cell limited model with NK cell class is practically identifiable, except for the rescaled half saturation constant. The within-host-within-fetus model has all fetus-related parameters not practically identifiable without data on the fetus, as well as the rescaled half saturation constant is also not practically identifiable. The remaining parameters are practically identifiable. Finally we find that none of the parameters of the within-vector model is practically identifiable.

Alzheimer's disease is a degenerative disorder characterized by the loss of synapses and neurons from the brain, as well as the accumulation of amyloid-based neuritic plaques. While it remains a matter of contention whether β-amyloid causes the neurodegeneration, β-amyloid aggregation is associated with the disease progression. Therefore, gaining a clearer understanding of this aggregation may help to better understand the disease. We develop a continuous-time model for β-amyloid aggregation using concepts from chemical kinetics and population dynamics. We show the model conserves mass and establish conditions for the existence and stability of equilibria. We also develop two discrete-time approximations to the model that are dynamically consistent. We show numerically that the continuous-time model produces sigmoidal growth, while the discrete-time approximations may exhibit oscillatory dynamics. Finally, sensitivity analysis reveals that aggregate concentration is most sensitive to parameters involved in monomer production and nucleation, suggesting the need for good estimates of such parameters.

Studies have shown that sexual transmission, both heterosexually and homosexually, is one of the main ways of HBV infection. Based on this fact, we propose a mathematical model to study the sexual transmission of HBV among adults by classifying adults into men and women and considering both same-sex and opposite-sex transmissions of HBV in adults. Firstly, we calculate the basic reproduction number $R_0$ and the disease-free equilibrium point $E_0$. Secondly, by analysing the sensitivity of $R_0$ in terms of model parameters, we find that the infection rate among people who have same-sex partners, the frequency of homosexual contact and the immunity rate of adults play important roles in the transmission of HBV. Moreover, we use our model to fit the reported data in China and forecast the trend of hepatitis B. Our results demonstrate that popularizing the basic knowledge of HBV among residents, advocating healthy and reasonable sexual life style, reducing the number of adult carriers, and increasing the immunization rate of adults are effective measures to prevent and control hepatitis B.

In this paper, we propose a model to assess the impacts of budget allocation for vaccination and awareness programs on the dynamics of infectious diseases. The budget allocation is assumed to follow logistic growth, and its per capita growth rate increases proportional to disease prevalence. An increment in per-capita growth rate of budget allocation due to increase in infected individuals after a threshold value leads to onset of limit cycle oscillations. Our results reveal that the epidemic potential can be reduced or even disease can be eradicated through vaccination of high quality and/or continuous propagation of awareness among the people in endemic zones. We extend the proposed model by incorporating a discrete time delay in the increment of budget allocation due to infected population in the region. We observe that multiple stability switches occur and the system becomes chaotic on gradual increase in the value of time delay.

We propose two models inspired by the COVID-19 pandemic: a coupled disease-human behaviour (or disease-game theoretic), and a coupled disease-human behaviour-economic model, both of which account for the impact of social-distancing on disease control and economic growth. The models exhibit rich dynamical behaviour including multistable equilibria, a backward bifurcation, and sustained bounded periodic oscillations. Analyses of the first model suggests that the disease can be eliminated if everybody practices full social-distancing, but the most likely outcome is some level of disease coupled with some level of social-distancing. The same outcome is observed with the second model when the economy is weaker than the social norms to follow health directives. However, if the economy is stronger, it can support some level of social-distancing that can lead to disease elimination.

In this paper, we investigate the combined effects of fear, prey refuge and additional food for predator in a predator-prey system with Beddington type functional response. We observe oscillatory behaviour of the system in the absence of fear, refuge and additional food whereas the system shows stable dynamics if anyone of these three factors is introduced. After analysing the behaviour of system with fear, refuge and additional food, we find that the system destabilizes due to fear factor whereas refuge and additional food stabilize the system by killing persistent oscillations. We extend our model by considering the fact that after sensing the chemical/vocal cue, prey takes some time for assessing the predation risk. The delayed system shows chaotic dynamics through multiple stability switches for increasing values of time delay. Moreover, we see the impact of seasonal change in the level of fear on the delayed as well as non-delayed system.

We introduce a compartmental host-vector model for dengue with two viral strains, temporary cross-immunity for the hosts, and possible secondary infections. We study the conditions on existence of endemic equilibria where one strain displaces the other or the two virus strains co-exist. Since the host and vector epidemiology follow different time scales, the model is described as a slow-fast system. We use the geometric singular perturbation technique to reduce the model dimension. We compare the behaviour of the full model with that of the model with a quasi-steady approximation for the vector dynamics. We also perform numerical bifurcation analysis with parameter values from the literature and compare the bifurcation structure to that of previous two-strain host-only models.

This note provides an elementary derivation of the basic reproduction number and the effective reproduction number from the discrete Kermack-McKendrick epidemic model. The derived formulae match those derived from the continuous version of the model; however, the derivation from discrete model is a bit more intuitive. The MATLAB functions for its calculation are given. A real case example is considered and the results are compared with those obtained by the R0 and the EpiEstim software packages.