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A time-delayed virus dynamic model is proposed with general monotonic incidence, different nonlinear CTL (cytotoxic T lymphocyte) responses [CTL elimination function p y g 1 (z) and CTL stimulation function c y g 2 (z) ], and immune impairment. Indeed, the different CTL responses pose challenges in obtaining the dissipativeness of the model. By constructing appropriate Lyapunov functionals with some detailed analysis techniques, the global stability results of all equilibria of the model are obtained. By the way, we point out that the partial derivative f v (x , 0) is increasing (but not necessarily strictly) in x > 0 for the general monotonic incidence f (x , v). However, some papers defaulted that the partial derivative was strictly increasing. Our main results show that if the basic reproduction number R 0 ≤ 1 , the infection-free equilibrium E 0 is globally asymptotically stable (GAS); if CTL stimulation function c y g 2 (z) = 0 for z = 0 and the CTL threshold parameter R 1 ≤ 1 < R 0 , then the immunity-inactivated infection equilibrium E 1 is GAS; if the immunity-activated infection equilibrium E + exists, then it is GAS. Two specific examples are provided to illustrate the applicability of the main results. The main results acquired in this paper improve or extend some of the existing results. [ABSTRACT FROM AUTHOR]

In this paper, a reaction–diffusion–chemotaxis HIV-1 model with a cytotoxic T lymphocyte (CTL) immune response and general sensitivity is investigated. We first prove the global classical solvability and L ∞ -boundedness for the considered model in a bounded domain with arbitrary spatial dimensions, which extends the previous existing results. Then, we apply the global existence result to the case with a linear proliferation immune response and an incidence rate. We study the spatiotemporal dynamics about the three types of spatially homogeneous steady states: infection-free steady state S 0 , CTL-inactivated infection steady state S 1 , and CTL-activated infection steady state S ∗. Our analyses indicate that S 0 is globally asymptotically stable if the basic reproduction number R 0 is less than 1; if R 0 is between 1 and a threshold, then S 1 is globally asymptotically stable. However, if R 0 is larger than the threshold, then the chemoattraction and chemorepulsion can destabilize S ∗ , and thus, a spatiotemporal pattern forms as the chemotactic sensitivity crosses certain critical values. We obtain two kinds of important patterns, which are induced by chemotaxis: stationary Turing pattern and irregular oscillatory pattern. We also find that different chemotactic response functions can affect system's dynamics. Based on some empirical parameter values, numerical simulations are given to illustrate the effectiveness of the theoretical predications. [ABSTRACT FROM AUTHOR]

In this paper, a new stochastic epidemic model is established and the dynamical behavior of its solutions is studied for this model. A deterministic epidemic model (ordinary differential equation) is first proposed by considering the isolation mechanism, and the transmission probability function is determined by a Wells–Riley model method to analyze the transmission in the quarantine. For this deterministic model, the basic reproduction number R 0 is computed and it is used to determine the existence of disease-free and positive equilibria. The linearized stability of the equilibria is also discussed by analyzing the distribution of eigenvalues of the linear system. Following that, a corresponding stochastic epidemic model is further established by introducing stochastic disturbance. Then, the extinction result of the model is derived also with the help of the basic reproduction number R 0 s. Furthermore, by applying the theory of Markov semigroups, it is proved that the densities of the distributions of the solutions can converge to an invariant density or sweeping under certain conditions. At last, some numerical simulations are provided and discussed to illustrate the practicability of the model and the obtained theoretical results. [ABSTRACT FROM AUTHOR]

The ongoing monkeypox outbreak that began in the UK has currently spread to every continent. Here, we use ordinary differential equations to build a nine-compartmental mathematical model to examine the dynamics of monkeypox transmission. The basic reproduction number for both humans ( R 0 h) and animals ( R 0 a) is obtained using the next-generation matrix technique. Depending on the values of R 0 h and R 0 a , we discovered that there are three equilibria. The current study also looks at the stability of all equilibria. We discovered that the model experiences transcritical bifurcation at R 0 a = 1 for any value of R 0 h and at R 0 h = 1 for R 0 a < 1. This is the first study that, to the best of our knowledge, has constructed and solved an optimal monkeypox control strategy while taking vaccination and treatment controls into consideration. The infected averted ratio and incremental cost-effectiveness ratio were calculated to evaluate the cost-effectiveness of all viable control methods. Using the sensitivity index technique, the parameters used in the formulation of R 0 h and R 0 a are scaled. [ABSTRACT FROM AUTHOR]

A fractional order susceptible–exposed–infected–quarantined–recovered model is established on the complex networks. We calculate a specific expression for the basic reproduction number R 0 , prove the existence and uniqueness with respect to the solution, and prove the Ulam–Hyers stability of the model. Using the Latin hypercube sampling-partial rank correlation coefficient method, the influence of parameters on the R 0 is analyzed. Based on the results of the analysis, the optimal control of the model is investigated as the control variables with vaccination rate and quarantine rate applying Pontryagin's minimum principle. The effects of α , degree of nodes, and network size on the model dynamics are simulated separately by the prediction correction method. [ABSTRACT FROM AUTHOR]

Bovine viral diarrhea (BVD) is a disease in cattle with complex transmission dynamics that causes substantial economic losses and affects animal welfare. The infection can be transient or persistent. The mostly asymptomatic persistently infected hosts are the main source for transmission of the virus. This characteristic makes it difficult to control the spreading of BVD. We develop a deterministic compartmental model for the spreading dynamics of BVD within a herd and derive the basic reproduction number. This epidemiological quantity indicates that identification and removal of persistently infected animals is a successful control strategy if the transmission rate of transiently infected animals is small. Removing persistently infected animals from the herd at birth results in recurrent outbreaks with decreasing peak prevalence. We propose a stochastic version of the compartmental model that includes stochasticity in the transmission parameters. This stochasticity leads to sustained oscillations in cases where the deterministic model predicts oscillations with decreasing amplitude. The results provide useful information for the design of control strategies. [ABSTRACT FROM AUTHOR]