In this paper, a previous tumour–immune interaction model is simplified by neglecting a relatively weak direct immune activation by the tumour cells, which can still keep the essential dynamics properties of the original model. As the immune activation process is not instantaneous, we now incorporate one delay for the activation of the effector cells (ECs) by helper T cells (HTCs) into the model. Furthermore, we investigate the stability and instability regions of the tumour-presence equilibrium state of the delay-induced system with respect to two parameters, the activation rate of ECs by HTCs and the HTCs stimulation rate by the presence of identified tumour antigens. We show the dual role of this delay that can induce stability switches exhibiting destabilization as well as stabilization of the tumour-presence equilibrium. Besides, our results reveal that an appropriate immune activation time delay plays a significant role in control of tumour growth.

In this paper, we propose a latent HIV infection model with general incidence function and multiple delays. We derive the positivity and boundedness of solutions, as well as the existence and local stability of the infection-free and infected equilibria. By constructing Lyapunov functionals, we establish the global stability of the equilibria based on the basic reproduction number. We further study the global dynamics of this model with Holling type-Ⅱ incidence function through numerical simulations. Our results improve and generalize some existing ones. The results show that the prolonged time delay period of the maturation of the newly produced viruses may lead to the elimination of the viruses.