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More than 20 outbreaks of Ebola virus disease have occurred in Africa since 1976, and yet no adequate treatment is available. Hence, prevention, control measures and supportive treatment remain the only means to avoid the disease. Among these measures, contact tracing occupies a prominent place. In this paper, we propose a simple mathematical model that incorporates imperfect contact tracing, quarantine and hospitalization (or isolation). The control reproduction number ${{ℛ}}_c$ of each sub-model and for the full model are computed. Theoretically, we prove that when ${{ℛ}}_c$ is less than one, the corresponding model has a unique globally asymptotically stable disease-free equilibrium. Conversely, when ${{ℛ}}_c$ is greater than one, the disease-free equilibrium becomes unstable and a unique globally asymptotically stable endemic equilibrium arises. Furthermore, we numerically support the analytical results and assess the efficiency of different control strategies. Our main observation is that, to eradicate EVD, the combination of high contact tracing (up to 90%) and effective isolation is better than all other control measures, namely: (1) perfect contact tracing, (2) effective isolation or full hospitalization, (3) combination of medium contact tracing and medium isolation.

We study the reaction–diffusion Ebola PDE model that consists of equations that govern the evolution of susceptible, infected, recovered and deceased human individuals, as well as Ebola virus pathogens in the environment, with diffusive terms in all except the equation of the deceased human individuals. Under the setting of a spatial domain that is bounded, we prove the global well-posedness of the system; in contrast to the previous work on similar models such as cholera, avian influenza, malaria and dengue fever, diffusion coefficients may be different. Moreover, we derive its basic reproduction number, and under the condition that the diffusion coefficients of the susceptible and infected hosts are same, we prove the global stability of the disease-free-equilibrium, and uniform persistence in cases when the basic reproduction number lies beneath and above one, respectively. Again, we do not require that the diffusion coefficients of the recovered hosts be the same as the diffusion coefficients of the susceptible and infected hosts, in contrast to previous work on other models of infectious diseases. Another technical difficulty in our model is that the solution semiflow is not compact due to the lack of diffusion in the equation of the deceased human individuals; we overcome this difficulty using functional analysis techniques concerning Kuratowski measure of non-compactness.