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In this paper, we introduce ordinary and delay differential equations to describe the interactions between a malignant tumour and the immune systemin vivoin the presence of human immunodeficiency virus (HIV) infection of CD4+T-cells. In the delay model, we take into account the time lags required by the healthy effector cell components to recognize the pathogens and tumour cells. The models consist of four populations: tumour cells, healthy effector cells (CD4+T-cells), effector cells infected by HIVs and free viral particles. The presence of delay term in the model leads to a notable increase in the complexity of the observed behaviour. We investigate the qualitative behaviour of the models and find the conditions that guarantee the asymptotic stability of the steady states. Numerical simulations are provided to illustrate and extend the theoretical results. The obtained results are consistent with the real phenomena and give a better understanding of cancer immunity and viral oncogenesis. [ABSTRACT FROM PUBLISHER]

This paper deals with stability and Hopf bifurcation analyses of a mathematical model of HIV infection of CD4+ T-cells. The model is based on a system of delay differential equations with logistic growth term and antiretroviral treatment with a discrete time delay, which plays a main role in changing the stability of each steady state. By fixing the time delay as a bifurcation parameter, we get a limit cycle bifurcation about the infected steady state. We study the effect of the time delay on the stability of the endemically infected equilibrium. We derive explicit formulae to determine the stability and direction of the limit cycles by using center manifold theory and normal form method. Numerical simulations are presented to illustrate the results. [ABSTRACT FROM AUTHOR]