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In this paper, we study a modified SIRI model without vital dynamics, based on a system of nonlinear ordinary differential equations, for epidemics that exhibit partial immunity after infection, reinfection, and disease-induced death. This model can be applied to study epidemics caused by SARS-CoV, MERS-CoV, and SARS-CoV-2 coronaviruses, since there is the possibility that, in diseases caused by these pathogens, individuals recovered from the infection have a decrease in their immunity and can be reinfected. On the other hand, it is known that, in populations infected by these coronaviruses, individuals with comorbidities or older people have significant mortality rates or deaths induced by the disease. By means of qualitative methods, we prove that such system has an endemic equilibrium and an infinite line of nonhyperbolic disease-free equilibria, we determine the local and global stability of these equilibria, and we also show that it has no periodic orbits. Furthermore, we calculate the basic reproductive number R 0 and find that the system exhibits a forward bifurcation: disease-free equilibria are stable when R 0 < 1 / σ and unstable when R 0 > 1 / σ , while the endemic equilibrium consist of an asymptotically stable upper branch that appears from R 0 > 1 / σ , σ being the rate that quantifies reinfection. We also show that this system has two conserved quantities. Additionally, we show some of the most representative numerical solutions of this system. [ABSTRACT FROM AUTHOR]

We study an epidemiological mathematical model formulated in terms of an ODE system taking into account both social and nonsocial contagion risks of obesity. Analyzing first the case in which the model presents only the effect due to social contagion and using qualitative methods of the stability analysis, we prove that such system has at the most three equilibrium points, one disease-free equilibrium and two endemic equilibria, and also that it has no periodic orbits. Particularly, we found that when considering R0 (the basic reproductive number) as a parameter, the system exhibits a backward bifurcation: the disease-free equilibrium is stable when R0<1 and unstable when R0>1, whereas the two endemic equilibria appear from R0⁎ (a specific positive value reached by R0 and less than unity), one being asymptotically stable and the other unstable, but for R0>1 values, only the former remains inside the feasible region. On the other hand, considering social and nonsocial contagion and following the same methodology, we found that the dynamic of the model is simpler than that described above: it has a unique endemic equilibrium point that is globally asymptotically stable. [ABSTRACT FROM AUTHOR]

The aim of this paper is to model the dynamics of the human papillomavirus (HPV) in cervical epithelial cells. We developed a mathematical model of the epithelial cellular dynamics of the stratified epithelium of three (basale, intermedium, and corneum) stratums that is based on three ordinary differential equations. We determine the biological condition for the existence of the epithelial cell homeostasis equilibrium, and we obtain the necessary and sufficient conditions for its global stability using the method of Lyapunov functions and a theorem on limiting systems. We have also developed a mathematical model based on seven ordinary differential equations that describes the dynamics of HPV infection. We calculated the basic reproductive number ( R 0 ) of the infection using the next-generation operator method. We determine the existence and the local stability of the equilibrium point of the cellular homeostasis of the epithelium. We then give a sufficient condition for the global asymptotic stability of the epithelial cell homeostasis equilibrium using the Lyapunov function method. We proved that this equilibrium point is nonhyperbolic when R 0 = 1 and that in this case, the system presents a forward bifurcation, which shows the existence of an infected equilibrium point when R 0 > 1. We also study the solutions numerically (i.e., viral kinetic in silico) when R 0 > 1. Finally, local sensitivity index was calculated to assess the influence of different parameters on basic reproductive number. Our model reproduces the transient, acute, latent, and chronic infections that have been reported in studies of the natural history of HPV. [ABSTRACT FROM AUTHOR]