DIMACS 10/9/06 Zhilan Feng Collaborators and references Zhilan Feng, David Smith, F. Ellis McKenzie, Simon Levin Mathematical Biosciences (2004) Zhilan Feng, Yingfei Yi, Huaiping Zhu J. Dynamics and Differential Equations (2004) Zhilan Feng, Carlos Castillo-Chavez Mathematical Biosciences and Engineering (2006) Coupling ecology and evolution: malaria and the S-gene across time scales Zhilan Feng, Department of Mathematics, Purdue University
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DIMACS 10/9/06 Zhilan Feng Collaborators and references Zhilan Feng, David Smith, F. Ellis McKenzie, Simon Levin Mathematical Biosciences (2004) Zhilan.
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DIMACS 10/9/06
Zhilan Feng
Collaborators and references
Zhilan Feng, David Smith, F. Ellis McKenzie, Simon Levin
Mathematical Biosciences (2004)
Zhilan Feng, Yingfei Yi, Huaiping Zhu
J. Dynamics and Differential Equations (2004)
Zhilan Feng, Carlos Castillo-Chavez
Mathematical Biosciences and Engineering (2006)
Coupling ecology and evolution: malaria and the S-gene across time scales
Zhilan Feng, Department of Mathematics, Purdue University
DIMACS 10/9/06
Zhilan Feng
Outline
Malaria epidemiology and the sickle-cell gene
An endemic model of malaria without genetics
A population genetics model without epidemics
A model coupling epidemics and S-gene dynamics
Analysis of the model
Discussion
DIMACS 10/9/06
Zhilan Feng
Malaria and the sickle-cell gene
Malaria has long been a scourge to humans. The exceptionally high mortality in some regions has led to strong selection for resistance, even at the cost of increased risk of potentially fatal red blood cell deformities in some offspring. Genes that confer resistance to malaria when they appear in heterozygous individuals are known to lead to sickle-cell anemia, or other blood diseases, when they appear in homozygous form.
Thus, there is balancing selection against the evolution of resistance, with the strength of that selection dependent upon malaria prevalence.
Over longer time scales, the increased frequency of resistance may decrease the prevalence of malaria and reduce selection for resistance
However, possession of the sickle-cell gene leads to longer-lasting parasitaemia in heterozygote individuals, and therefore the presence of resistance may actually increase infection prevalence We explore the interplay among these processes, operating over very different time scales