Struchiner C J, Halloran M E, Spielman A
Math Biosci. 1989 May;94(1):87-113. doi: 10.1016/0025-5564(89)90073-4.
Starting from a modification of the model of malaria transmission developed for the Garki project, this paper develops a model containing variables relevant to the stimulation of malaria vaccination programs. Modifications include (1) integration of maintenance of immunity dependent on boosting and the possibility of loss of immunity; (2) introduction of a boosting factor distinct from susceptibility to infection; (3) reinterpretation of the epidemiological compartments of positive immunes and nonimmunes in terms of severity of disease rather than just infection; (4) interpretation of the different stage-specific levels of immunity; (5) discrimination between different susceptibilities for the immune and nonimmune classes; (6) reformulation of the expression for acquisition of immunity to be biologically more acceptable. Simulations using the Garki model, Nedelman's modification of it, and our Basic model compare the similarities and differences in the predictive behavior of the models. Simulations using the Basic model reproduce observed periodic fluctuations of malaria attributed to the interplay of transmission-blocking immunity and loss of immunity in the absence of boosting in areas of unstable malaria transmission.
本文从为加基项目开发的疟疾传播模型的一种改进出发，构建了一个包含与疟疾疫苗接种计划刺激相关变量的模型。改进包括：（1）整合依赖加强免疫维持的免疫力以及免疫力丧失的可能性；（2）引入一个与感染易感性不同的加强因子；（3）根据疾病严重程度而非仅仅感染情况重新解释阳性免疫者和非免疫者的流行病学分类；（4）解释不同阶段特异性免疫水平；（5）区分免疫类和非免疫类的不同易感性；（6）重新表述免疫获得的表达式，使其在生物学上更易接受。使用加基模型、内德尔曼对其的改进以及我们的基础模型进行的模拟，比较了各模型预测行为的异同。使用基础模型进行的模拟再现了在不稳定疟疾传播地区，由于在没有加强免疫的情况下传播阻断免疫力和免疫力丧失之间的相互作用而观察到的疟疾周期性波动。
