Journal of Biological Dynamics最新文献

Human T-lymphotropic virus (HTLV) and human immunodeficiency virus (HIV) are two retroviruses that pose a certain threat to human psychology and physiology. In this paper, we propose a diffusive HTLV and HIV coinfection model with macrophages, two delays, cell-to-cell transmission and three latently infected cells in which latent HIV infected CD4${}^{+}$T cells, latent HIV infected macrophages, and latent HTLV infected CD4${}^{+}$T cells are considered. Four reproduction number and four equilibria, namely, infection-free equilibrium, HIV infection equilibrium, HTLV infection equilibrium and HTLV and HIV coinfection equilibrium, are calculated and proved the global asymptotic stability of the coinfection model. Numerical simulations are executed to showcase the corresponding theoretical outcomes and uncover how macrophages and latently infected cells influence the dynamics of HTLV and HIV coinfection.

In this paper, we analyze a deterministic model of malaria and Corona Virus Disease 2019 co-infection within a homogeneous population. We first studied the single infection model of each disease and then the co-infection dynamics. We calculate the basic reproduction number of each model and study the existence and stability of the steady states. Then, we show that under some suitable conditions, both the malaria single infection model and co-infection model exhibit backward bifurcation. Furthermore, we analyze the conditions of extinction, competitive exclusion and co-existence of these two diseases. In addition, a local sensitivity analysis of the basic reproduction numbers is performed to explore the impact of the different parameters' variability on the dynamics of each disease. Moreover, we apply Pontryagin's maximum principle to determine optimal strategies to control the two diseases in case of co-infection. Finally, some numerical simulation results are presented to support the theoretical findings.

The global dynamic behavior of the respiration process in bacterial culture at different concentrations was comprehensively described using the qualitative theory of differential equations and symbolic calculation software.

This paper examines a three-species ecological competition model with two predators and one prey, incorporating food-limited growth and both linear and quadratic harvesting strategies. Using mathematical analysis, we identify equilibrium points and derive conditions for their stability and persistence. The results reveal that quadratic harvesting significantly enhances stability, promotes coexistence, and mitigates extinction risks compared to linear harvesting. Numerical simulations validate the theoretical findings, highlighting the effectiveness of quadratic harvesting in managing population dynamics. These insights contribute to the mathematical understanding of sustainable harvesting strategies in complex ecological systems.

In this paper, we establish a compartmental model in which the transmission rate is associated with the fear of being infected by COVID-19. We provide a detailed analysis of the epidemic model and established results for the existence of a positively invariant set. The expression of the basic reproduction number $R_0$ is characterized. It is shown that the disease-free equilibrium (DFE) is globally asymptotically stable if $R_0<1$, and the system exhibits a forward bifurcation if $R_0=1$. When $R_0>1$, the system is uniformly persistent, the DFE is unstable and there exists a unique and globally asymptotic stable endemic equilibrium (EE). We fit unknown parameters using the reported data in Canada from September 1 to October 10, 2021, and carry out sensitivity analysis. The quantitative analysis of the model with awareness demonstrates the significance of reducing the transmission rate and enhancing public protective awareness.

In this work, the intricacies and complexities of dynamical properties are extensively studied for the proposed deterministic and stochastic prey-predator models. The influence of fear effects, prey refuge and feedback control are considered and thorough theoretical research is conducted on the systems. It commences by establishing the global stability and uniqueness of the positive equilibrium of the deterministic model. Then for the stochastic system, the existence, uniqueness and boundedness of a global positive solution are analysed by constructing appropriate Lyapunov functions. Sufficient conditions are established for the extinction and persistence of the stochastic model. It can be observed that both the fear effect and prey refuge have a greatly impact on the dynamics of system. Intermediate values of feedback control intensity may be the most beneficial to species coexistence. It provides new insights into the sustainability of ecosystems.

This study presents a mathematical model to explore malaria transmission dynamics in the presence of antimalarial drug-resistant parasites and insecticide-resistant mosquitoes. The analytical findings demonstrate a stable disease-free equilibrium when the effective reproduction number is below one. For single-strain malaria infections, the endemic equilibrium may exhibit one, two or no solutions. The model is extended to incorporate three time-dependent controls: long-lasting insecticidal nets, antimalarial treatment and mosquito adulticides. Simulation results indicate that interventions excluding drug-resistant parasites and insecticide-resistant mosquitoes are ineffective. The most effective strategies combine insecticides targeting all vectors with treatments for all malaria cases, regardless of resistance. Efficiency analysis suggests implementing all three controls at $\ge 80\%$ efficacy for the maximum impact, while assessments of cost-effectiveness highlight the combination of long-lasting insecticidal nets and antimalarial treatment as a practical option in resource-constrained settings. Nonetheless, integrating all three measures is recommended for substantial malaria transmission reduction.

This paper proposes an immunosuppressive infection model with time delay and stochastic perturbation. A stochastic threshold $R_0^s$ is constructed, and the sufficient conditions for virus extinction and weak persistence are given. Subsequently, we respectively fit the SDDE and ODE models to the real data, and conduct a sensitivity analysis of the equilibrium. The greater the noise intensity, the more obvious the oscillation amplitude of the solution curve around the immune-free equilibrium, the larger noise intensity can cause the originally persistent virus in ODE to go extinct in the SDDE model. The greater the time delay, the longer it takes for the virus and immune cells to reach their first peaks. The viral replication rate significantly affects the virus-immune system, and the reproduction of HIV-1 can be inhibited by modulating it. A relatively high viral inhibition rate will lead to the extinction of immune cells while the virus persists.

Chemical control is crucial in pest management, but delayed responses to pesticide application can significantly affect its success. This study develops a type of novel mathematical models combining delayed impulse differential equations with pulse pesticide spraying to evaluate these delayed effects. The uniform stability of the pest eradication solution is analysed, and key parameters influencing pest control success are explored. Considering delays in both pest population growth reaching environmental capacity and pesticide response, a double delayed impulse differential equation is formulated. The asymptotic stability and exponential stability of the system are studied, and threshold conditions for pest extinction are identified. The findings help optimize pest control strategies under delayed pesticide responses.

We use mathematical modeling to study the proliferation dynamics of CD4+ T cells within an immune response. This proliferation is driven by the autocrine reaction of helper T cells and interleukin-2 (IL-2), and regulated by natural regulatory T cells (nTregs). Previous studies suggested that a fratricidal mechanism is necessary to eliminate helper T cells post-infection. Contrary to this, our mathematical analysis establishes that the depletion of these cells is due to two pivotal factors: the saturation in the proliferation rate of helper CD4+ T cells at high IL-2 concentrations, and the activation rate of nTregs outpacing their death rate. This yields an excitable process, such that the proliferation starts once the helper T cell population passes a threshold. Additionally, we find that when the proliferation of nTregs lags behind their mortality, induced regulatory T cells (iTregs) are crucial to curbing the proliferation of helper CD4+ T cells.