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

TL;DR

This study analyzes a virus infection model with antibody and CTL responses, showing that boosting CTL responses relative to antibody responses can stabilize infection control, informing vaccine strategies.

Contribution

It provides a stability analysis of a within-host virus model, revealing the importance of balancing immune responses to control persistent infections.

Findings

Equilibria undergo at most two transcritical bifurcations.

Boosting CTL responses over antibody responses stabilizes the endemic equilibrium.

Results suggest vaccines should moderate antibody responses to enhance CTL activity.

Abstract

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