Bifurcations and Bistability of an Age-Structured Viral Infection Model with a Nonmonotonic Immune Response

Abstract

Recent studies have demonstrated that immune impairment is an essential factor in viral infection for disease development and treatment. In this paper, we formulate an age-structured viral infection model with a nonmonotonic immune response and perform dynamical analysis to explore the effects of both immune impairment and virus control. The basic infection reproduction number is derived for a general viral production rate, which determines the global stability of the infection-free equilibrium. For the immune intensity, we get two important thresholds, the post-treatment control threshold and the elite control threshold. The interval between the two thresholds is a bistable interval, where there are two immune-present infected equilibria. When the immune intensity is greater than the elite control threshold, only one immune-present infected equilibrium exists and it is stable. By assuming the death rate and virus production rate of infected cells to be constants, with the immune intensity as a bifurcation parameter, the system exhibits saddle-node bifurcation, transcritical bifurcation, and backward/forward bifurcation.