Reluga Timothy C, Medlock Jan, Perelson Alan S
Theoretical Biology and Biophysics Group, Theoretical Division, Los Alamos National Laboratory, Los Alamos, NM 87545, USA.
J Theor Biol. 2008 May 7;252(1):155-65. doi: 10.1016/j.jtbi.2008.01.014. Epub 2008 Jan 26.
Many disease pathogens stimulate immunity in their hosts, which then wanes over time. To better understand the impact of this immunity on epidemiological dynamics, we propose an epidemic model structured according to immunity level that can be applied in many different settings. Under biologically realistic hypotheses, we find that immunity alone never creates a backward bifurcation of the disease-free steady state. This does not rule out the possibility of multiple stable equilibria, but we provide two sufficient conditions for the uniqueness of the endemic equilibrium, and show that these conditions ensure uniqueness in several common special cases. Our results indicate that the within-host dynamics of immunity can, in principle, have important consequences for population-level dynamics, but also suggest that this would require strong non-monotone effects in the immune response to infection. Neutralizing antibody titer data for measles are used to demonstrate the biological application of our theory.
许多疾病病原体可刺激其宿主产生免疫反应,而这种免疫反应会随着时间逐渐减弱。为了更好地理解这种免疫对流行病学动态的影响,我们提出了一种根据免疫水平构建的流行病模型,该模型可应用于许多不同的场景。在符合生物学实际的假设下,我们发现仅免疫因素永远不会导致无病稳态出现反向分岔。这并不排除存在多个稳定平衡点的可能性,但我们给出了地方病平衡点唯一性的两个充分条件,并表明这些条件在几种常见的特殊情况下可确保唯一性。我们的结果表明,宿主内部的免疫动态原则上可能对种群水平的动态产生重要影响,但也表明这需要免疫反应对感染有强烈的非单调效应。麻疹的中和抗体滴度数据被用于证明我们理论的生物学应用。