Book contents
- Frontmatter
- Contents
- Introduction
- Participants
- Non-Participant Contributors
- Part 1 Transmissible diseases with long development times and vaccination strategies
- Part 2 Dynamics of immunity (development of disease within individuals)
- Evolutionary dynamics of HIV infections
- Statistical models for analysis of longitudinal, CD4 data
- Some mathematical and statistical issues in assessing the evidence for acquired immunity to schistosomiasis
- Virulence and transmissibility in P. falciparum malaria
- Invited Discussion
- Invited Discussion
- Invited Discussion
- Lifespan of human T lymphocytes
- Diversity and virulence thresholds in AIDS
- Statistical analysis of AZT effect on CD4 cell counts in HIV disease
- Modeling progression of HIV infection: staging and the Chicago MACS cohort
- The interpretation of immunoepidemiological data for helminth infections
- The distribution of malaria parasites in the mosquito vector: consequences for assessing infection intensity in the field
- When susceptible and infective human hosts are not equally attractive to mosquitoes: a generalisation of the Ross malaria model
- The dynamics of blood stage malaria: modelling strain specific and strain transcending immunity
- Part 3 Population heterogeneity (mixing)
- Part 4 Consequences of treatment interventions
- Part 5 Prediction
The dynamics of blood stage malaria: modelling strain specific and strain transcending immunity
Published online by Cambridge University Press: 04 August 2010
- Frontmatter
- Contents
- Introduction
- Participants
- Non-Participant Contributors
- Part 1 Transmissible diseases with long development times and vaccination strategies
- Part 2 Dynamics of immunity (development of disease within individuals)
- Evolutionary dynamics of HIV infections
- Statistical models for analysis of longitudinal, CD4 data
- Some mathematical and statistical issues in assessing the evidence for acquired immunity to schistosomiasis
- Virulence and transmissibility in P. falciparum malaria
- Invited Discussion
- Invited Discussion
- Invited Discussion
- Lifespan of human T lymphocytes
- Diversity and virulence thresholds in AIDS
- Statistical analysis of AZT effect on CD4 cell counts in HIV disease
- Modeling progression of HIV infection: staging and the Chicago MACS cohort
- The interpretation of immunoepidemiological data for helminth infections
- The distribution of malaria parasites in the mosquito vector: consequences for assessing infection intensity in the field
- When susceptible and infective human hosts are not equally attractive to mosquitoes: a generalisation of the Ross malaria model
- The dynamics of blood stage malaria: modelling strain specific and strain transcending immunity
- Part 3 Population heterogeneity (mixing)
- Part 4 Consequences of treatment interventions
- Part 5 Prediction
Summary
There is a great deal of interest among malariologists about the effect of antigenic diversity on the transmission dynamics of malaria (Day and Marsh 1991). Complementing other modelling studies on this effect at a population level (Gupta et al. 1994), we explore the within-host dynamics of blood stage malaria in a single individual infected with a basket of different parasite strains. By generalising a previous model (Anderson et al. 1989) to account for this situation and calibrating it against the observed data on the time course of malaria infection, we are able to include the effects of the host immune response despite the difficulty of obtaining quantitative data on this component.
We intend to use our model to investigate the effects of different types of immune response: for example the relative success of a fast, quickly decaying strain-specific response combined with a slowly generated but persistent strain-transcending response.
We will discuss whether combinations of strain specific and strain transcending responses to a basket of infections at the blood stage of malaria account for the observed patterns of parasitaemia in malaria endemic areas.
Following Anderson et al. (1989), and similarly to Hellriegel (1992), we define x(t) as the number of uninfected erythrocytes, m(t) as the number of free merozoites and y(t) as the number of infected red blood cells. We assume that red blood cells are produced at a constant rate Λ and die at a per-capita rate μ with a mean life-span of l/μ. Free merozoites infect unparasitised cells at a rate βxm; these cells rupture after a mean time of 1/α to produce r more free merozoites.
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- Information
- Models for Infectious Human DiseasesTheir Structure and Relation to Data, pp. 210 - 212Publisher: Cambridge University PressPrint publication year: 1996
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