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We analyze a within-host model of virus infection with antibody and CD8+cytotoxic T lymphocyte (CTL) responses proposed by Schwartz et al. (2013). Thegoal of this work is to gain an overview of the stability of thebiologically-relevant equilibria as a function of the model's immune responseparameters. We show that the equilibria undergo at most two forwardtranscritical bifurcations. The model is also explored numerically and resultsare applied to equine infectious anemia virus infection. In order to arrive atstability of the biologically-relevant endemic equilibrium characterized bycoexistence of antibody and CTL responses, the parameters promoting CTLresponses need to be boosted over parameters promoting antibody production.This result may seem counter-intuitive (in that a weaker antibody response isbetter) but can be understood in terms of a balance between CTL and antibodyresponses that is needed to permit existence of CTLs. In conclusion, anintervention such as a vaccine that is intended to control a persistent viralinfection with both immune responses should moderate the antibody response toallow for stimulation of the CTL response.

A model of virus infection with immune responses supports boosting CTL response to balance antibody response