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A model for the origins and spread of drug-resistant malaria

Published online by Cambridge University Press:  01 August 1997

I. M. HASTINGS
I. M. HASTINGS
Affiliation:
Present address: Institute of Cell, Animal and Population Biology, University of Edinburgh, West Mains Road, Edinburgh EH9 3JT. Tel: +0131 650 5484. Fax: +0131 667 3210. E-mail: eang18@tattoo.ed.ac.uk. Laboratoire Génétique Moléculaire des Parasites et des Vecteurs, ORSTOM, 911 Av. Agropolis BP5045, 34032 Montpellier cedex 1, France
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Abstract

A general method of investigating parasite population genetics is presented and used to investigate the evolution of drug resistance in Plasmodium. The most important biological factor is the nature of the control, presumably through host immunity, of the malarial infection. Two models are examined: a ‘generalized immunity’ (GI) model in which immunity regulates the overall level of infection, and a ‘specific immunity’ (SI) model in which each clone within the infection is regulated independently. These models are used to investigate 3 critical factors in the evolution of resistance: (i) the frequency of resistant alleles in the population prior to drug use, (ii) the dynamics of resistance following drug application and (iii) the magnitude of threshold frequencies below which resistance will not evolve. These analyses also identify the implicit assumptions made in several previous models, reconcile their differing conclusions and allow a more informed debate about the practical application of drugs.

Keywords

drugevolutionimmunitymalariaPlasmodiumresistance
Type
Research Article
Information
Parasitology , Volume 115 , Issue 2 , August 1997 , pp. 133 - 141
Copyright
1997 Cambridge University Press

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