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Table 2 Overview and main immune dynamics of the models

From: Mechanistic within-host models of the asexual Plasmodium falciparum infection: a review and analytical assessment

General model structure, and parasite dynamics   
Models Molineaux et al.    Gatton & Cheng Eckhoff Childs & Buckee Gurarie et al. McKenzie and Bossert
Adapted models   Johnston et al.       
   Challenger et al.      
Assumptions on innate immune response Dependent on total parasite density at a given time Dependent on density of each parasites expressing variants for which there is no antibody response, and on the rupturing of iRBCs Dependent on total parasite density at a given time and is capped by a maximum efficacy term Dependent on iRBC density Dependent on cumulative asexual parasite density
Assumptions on variant specific immune response Dependent on the variant specific parasite density, and lasting in time with a decaying intensity Dependent on the total parasite within a time frame preceding the time of response, and on time after infection start Triggered by a variant specific parasite density threshold, dependent on the time after infection start, and the magnitude increases if the antibody has been produced previously Dependent on the variant specific parasite density Dependent on the variant specific parasite density, a maximum growth and decay rate, and is restricted by total number of immune cells available Not explicit, but adaptive immune response includes random falls due to implicit variant switching –
Assumptions on general adaptive immune response Depends on cumulative total parasite density Dependent on the time after the start of the infection Modelled as immune response against merozoite antigens, increase every 2 days, dependent on parasite density Dependent on cumulative number or days the total parasite population is above 107 Dependent on iRBC density and combined innate and adaptive effector pool Dependent on cumulative asexual parasite density, does not decay in time
Includes cross-reactivity No Not explicitly Yes, the variant specific response approximately kills 5% of all other variants Yes, response to variants randomly assigned to 5 subgroups Yes, response to variants randomly assigned to subgroups No Yes, immune response to one genotype can be activated by the presence of another genotype
Other comments Innate and adaptive immune response include patient specific parameters    Parameters differ with different parasite strains Immune memory is included in the model Detailed sensitivity analysis resulted in significant impact on the model’s outcome of small changes in parameter values, highlighting the challenged face by within host models   
  1. The model description includes the main characteristics of innate, variant specific, and general adaptive immune responses
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Malaria Journal

ISSN: 1475-2875

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