论文标题
具有免疫反应的病毒感染模型支持增强CTL反应以平衡抗体反应
A model of virus infection with immune responses supports boosting CTL response to balance antibody response
论文作者
论文摘要
我们分析了Schwartz等人提出的抗体和CD8+细胞毒性T淋巴细胞（CTL）反应的病毒感染的主宿主模型。 （2013）。这项工作的目的是概述与模型的免疫反应参数的函数，概述了生物学上的平衡的稳定性。我们表明，平衡最多在两个正向跨临界分叉中进行。该模型还进行了数值探索，并将结果应用于马传染性贫血病毒感染。为了达到以抗体和CTL响应共存为特征的生物相关的地方性平衡的稳定性，促进CTL响应的参数需要在促进抗体产生的参数上提高。该结果似乎是违反直觉的（因为较弱的抗体反应更好），但可以从CTL和允许存在CTL所需的抗体反应之间的平衡来理解。总之，旨在控制具有两种免疫反应的持续性病毒感染的疫苗等干预措施应适应抗体反应，以允许刺激CTL反应。
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.
