In this paper, we investigate a mathematical model of hematopoietic stem cell dynamics. We take two cell populations into account, quiescent and proliferating one, and we note the difference between dividing cells that enter directly to the quiescent phase and dividing cells that return to the proliferating phase to divide again. The resulting mathematical model is a system of two age-structured partial differential equations. By integrating this system over age and using the characteristics method, we reduce it to a delay differential-difference system, and we investigate the existence and stability of the steady states. We give sufficient conditions for boundedness and unboundedness properties for the solutions of this system. By constructing a Lyapunov function, the trivial steady state, describing cell's dying out, is proven to be globally asymptotically stable when it is the only equilibrium. The stability analysis of the unique positive steady state, the most biologically meaningful one, and the existence of a Hopf bifurcation allow the determination of a stability area, which is related to a delay-dependent characteristic equation. Numerical simulations illustrate our results on the asymptotic behavior of the steady states and show very rich dynamics of this model. This study may be helpful in understanding the uncontrolled proliferation of blood cells in some hematological disorders.

In this paper, we are concerned with an epidemic model of susceptible, infected and recovered (SIR) population dynamic by considering an age-structured phase of protection with limited duration, for instance due to vaccination or drugs with temporary immunity. The model is reduced to a delay differential-difference system, where the delay is the duration of the protection phase. We investigate the local asymptotic stability of the two steady states: disease-free and endemic. We also establish when the endemic steady state exists, the uniform persistence of the disease. We construct quadratic and logarithmic Lyapunov functions to establish the global asymptotic stability of the two steady states. We prove that the global stability is completely determined by the basic reproduction number.

Starting from an age structured partial differential model, constructed taking into account the mosquito life cycle and the main features of theWolbachia-infection, we derived a delay differential model using the method of characteristics, to study the colonization and persistence of theWolbachia-transinfectedAedes aegyptimosquito in an environment where the uninfected wild mosquito population is already established. Under some conditions, the model can be reduced to a Nicholson-type delay differential system; here, the delay represents the duration of mosquito immature phase that comprises egg, larva and pupa. In addition to mortality and oviposition rates characteristic of the life cycle of the mosquito, other biological features such as cytoplasmic incompatibility, bacterial inheritance, and deviation on sex ratio are considered in the model. The model presents three equilibriums: the extinction of both populations, the extinction ofWolbachia-infected population and persistence of uninfected one, and the coexistence. The conditions of existence for each equilibrium are obtained analytically and have been interpreted biologically. It is shown that the increase of the delay can promote, through Hopf bifurcation, stability switch towards instability for the nonzero equilibriums. Overall, when the delay increases and crosses predetermined thresholds, the populations go to extinction.

During the primary CD8 T-Cell immune response to an intracellular pathogen, CD8 T-Cells undergo exponential proliferation and continuous differentiation, acquiring cytotoxic capabilities to address the infection and memorize the corresponding antigen. After cleaning the organism, the only CD8 T-Cells left are antigen-specific memory cells whose role is to respond stronger and faster in case they are presented this very same antigen again. That is how vaccines work: a small quantity of a weakened pathogen is introduced in the organism to trigger the primary response, generating corresponding memory cells in the process, giving the organism a way to defend himself in case it encounters the same pathogen again. To investigate this process, we propose a non linear, multi-scale mathematical model of the CD8 T-Cells immune response due to vaccination using a maturity structured partial differential equation. At the intracellular scale, the level of expression of key proteins is modeled by a delay differential equation system, which gives the speeds of maturation for each cell. The population of cells is modeled by a maturity structured equation whose speeds are given by the intracellular model. We focus here on building the model, as well as its asymptotic study. Finally, we display numerical simulations showing the model can reproduce the biological dynamics of the cell population for both the primary response and the secondary responses.