Synchronization is one of the most striking instances of collective behavior, occurring in many natural phenomena. For example, in some ant species, ants are inactive within the nest most of the time, but their bursts of activity are highly synchronized and involve the entire nest population. Here we revisit a simulation model that generates this synchronized rhythmic activity through autocatalytic behavior, i.e., active ants can activate inactive ants, followed by a period of rest. We derive a set of delay differential equations that provide an accurate description of the simulations for large ant colonies. Analysis of the fixed-point solutions, complemented by numerical integration of the equations, indicates the existence of stable limit-cycle solutions when the rest period is greater than a threshold and the event of spontaneous activation of inactive ants is very unlikely, so that most of the arousal of ants is done by active ants. Furthermore, we argue that the persistent oscillations observed in the simulations for colonies of finite size are due to resonant amplification of demographic noise.

Many neurodegenerative diseases (NDs) are characterized by the slow spatial spread of toxic protein species in the brain. The toxic proteins can induce neuronal stress, triggering the Unfolded Protein Response (UPR), which slows or stops protein translation and can indirectly reduce the toxic load. However, the UPR may also trigger processes leading to apoptotic cell death and the UPR is implicated in the progression of several NDs. In this paper, we develop a novel mathematical model to describe the spatiotemporal dynamics of the UPR mechanism for prion diseases. Our model is centered around a single neuron, with representative proteins P (healthy) and S (toxic) interacting with heterodimer dynamics (S interacts with P to form two S\'s). The model takes the form of a coupled system of nonlinear reaction-diffusion equations with a delayed, nonlinear flux for P (delay from the UPR). Through the delay, we find parameter regimes that exhibit oscillations in the P- and S-protein levels. We find that oscillations are more pronounced when the S-clearance rate and S-diffusivity are small in comparison to the P-clearance rate and P-diffusivity, respectively. The oscillations become more pronounced as delays in initiating the UPR increase. We also consider quasi-realistic clinical parameters to understand how possible drug therapies can alter the course of a prion disease. We find that decreasing the production of P, decreasing the recruitment rate, increasing the diffusivity of S, increasing the UPR S-threshold, and increasing the S clearance rate appear to be the most powerful modifications to reduce the mean UPR intensity and potentially moderate the disease progression.

Delays and stochasticity have both served as crucially valuable ingredients in mathematical descriptions of control, physical and biological systems. In this work, we investigate how explicitly dynamical stochasticity in delays modulates the effect of delayed feedback. To do so, we consider a hybrid model where stochastic delays evolve by a continuous-time Markov chain, and between switching events, the system of interest evolves via a deterministic delay equation. Our main contribution is the calculation of an effective delay equation in the fast switching limit. This effective equation maintains the influence of all subsystem delays and cannot be replaced with a single effective delay. To illustrate the relevance of this calculation, we investigate a simple model of stochastically switching delayed feedback motivated by gene regulation. We show that sufficiently fast switching between two oscillatory subsystems can yield stable dynamics.

A four-dimensional delay differential equations (DDEs) model of malaria with standard incidence rate is proposed. By utilizing the limiting system of the model and Lyapunov direct method, the global stability of equilibria of the model is obtained with respect to the basic reproduction number R 0. Specifically, it shows that the disease-free equilibrium E 0 is globally asymptotically stable (GAS) for R 0 < 1, and globally attractive (GA) for R 0 = 1, while the endemic equilibrium E* is GAS and E 0 is unstable for R 0 > 1. Especially, to obtain the global stability of the equilibrium E* for R 0 > 1, the weak persistence of the model is proved by some analysis techniques.

In this work, we briefly describe our technology developed for computing periodic solutions of time-delay systems and discuss the results of computing periodic solutions for the Marchuk-Petrov model with parameter values, corresponding to hepatitis B infection. We identified the regions in the model parameter space in which an oscillatory dynamics in the form of periodic solutions exists. The respective solutions can be interpreted as active forms of chronic hepatitis B. The period and amplitude of oscillatory solutions were traced along the parameter determining the efficacy of antigen presentation by macrophages for T- and B-lymphocytes in the model.. The oscillatory regimes are characterized by enhanced destruction of hepatocytes as a consequence of immunopathology and temporal reduction of viral load to values which can be a prerequisite of spontaneous recovery observed in chronic HBV infection. Our study presents a first step in a systematic analysis of the chronic HBV infection using Marchuk-Petrov model of antiviral immune response.

Gamma distributed delay differential equations (DDEs) arise naturally in many modelling applications. However, appropriate numerical methods for generic gamma distributed DDEs have not previously been implemented. Modellers have therefore resorted to approximating the gamma distribution with an Erlang distribution and using the linear chain technique to derive an equivalent system of ordinary differential equations (ODEs). In this work, we address the lack of appropriate numerical tools for gamma distributed DDEs in two ways. First, we develop a functional continuous Runge-Kutta (FCRK) method to numerically integrate the gamma distributed DDE without resorting to Erlang approximation. We prove the fourth-order convergence of the FCRK method and perform numerical tests to demonstrate the accuracy of the new numerical method. Nevertheless, FCRK methods for infinite delay DDEs are not widely available in existing scientific software packages. As an alternative approach to solving gamma distributed DDEs, we also derive a hypoexponential approximation of the gamma distributed DDE. This hypoexponential approach is a more accurate approximation of the true gamma distributed DDE than the common Erlang approximation but, like the Erlang approximation, can be formulated as a system of ODEs and solved numerically using standard ODE software. Using our FCRK method to provide reference solutions, we show that the common Erlang approximation may produce solutions that are qualitatively different from the underlying gamma distributed DDE. However, the proposed hypoexponential approximations do not have this limitation. Finally, we apply our hypoexponential approximations to perform statistical inference on synthetic epidemiological data to illustrate the utility of the hypoexponential approximation.

In this paper, we discuss a framework for the polynomial approximation to the solution of initial value problems for differential equations. The framework is based on an expansion of the vector field along an orthonormal basis, and relies on perturbation results for the considered problem. Initially devised for the approximation of ordinary differential equations, it is here further extended and, moreover, generalized to cope with constant delay differential equations. Relevant classes of Runge-Kutta methods can be derived within this framework.

Most plant viral infections are vector-borne. There is a latent period of disease inside the vector after obtaining the virus from the infected plant. Thus, after interacting with an infected vector, the plant demonstrates an incubation time before becoming diseased. This paper analyzes a mathematical model for persistent vector-borne viral plant disease dynamics. The backpropagated neural network based on the Levenberg-Marquardt algorithm (NN-BLMA) is used to study approximate solutions for fluctuations in natural plant mortality and vector mortality rates. A state-of-the-art numerical technique is utilized to generate reference data for obtaining surrogate solutions for multiple cases through NN-BLMA. Curve fitting, regression analysis, error histograms, and convergence analysis are used to assess accuracy of the calculated solutions. It is evident from our simulations that NN-BLMA is accurate and reliable.

In the wake of the 2020 COVID-19 epidemic, much work has been performed on the development of mathematical models for the simulation of the epidemic and of disease models generally. Most works follow the susceptible-infected-removed (SIR) compartmental framework, modeling the epidemic with a system of ordinary differential equations. Alternative formulations using a partial differential equation (PDE) to incorporate both spatial and temporal resolution have also been introduced, with their numerical results showing potentially powerful descriptive and predictive capacity. In the present work, we introduce a new variation to such models by using delay differential equations (DDEs). The dynamics of many infectious diseases, including COVID-19, exhibit delays due to incubation periods and related phenomena. Accordingly, DDE models allow for a natural representation of the problem dynamics, in addition to offering advantages in terms of computational time and modeling, as they eliminate the need for additional, difficult-to-estimate, compartments (such as exposed individuals) to incorporate time delays. In the present work, we introduce a DDE epidemic model in both an ordinary and partial differential equation framework. We present a series of mathematical results assessing the stability of the formulation. We then perform several numerical experiments, validating both the mathematical results and establishing model\'s ability to reproduce measured data on realistic problems.

Many studies have shown that periodic erythrocytic (red blood cell linked) diseases are extremely rare in humans. To explain this observation, we develop here a simple model of erythropoiesis in mammals and investigate its stability in the parameter space. A bifurcation analysis enables us to sketch stability diagrams in the plane of key parameters. Contrary to some other mammal species such as rabbits, mice or dogs, we show that human-specific parameter values prevent periodic oscillations of red blood cells levels. In other words, human erythropoiesis seems to lie in a region of parameter space where oscillations exclusively concerning red blood cells cannot appear. Further mathematical analysis show that periodic oscillations of red blood cells levels are highly unusual and if exist, might only be due to an abnormally high erythrocytes destruction rate or to an abnormal hematopoietic stem cell commitment into the erythrocytic lineage. We also propose numerical results only for an improved version of our approach in order to give a more realistic but more complex approach of our problem.