Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654346
Title: Evolutionary genetics of malaria parasites
Author: Mackinnon, Margaret J.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1998
Availability of Full Text:
Access from EThOS:
Full text unavailable from EThOS. Please try the link below.
Access from Institution:
Abstract:
Two empirical studies on parasite virulence using the laboratory model of the rodent malaria parasite, Plasmodium chabaudi, in inbred mice, were conducted. In the first, the average virulence and transmissibility in eight parasite clones obtained from the wild were measured over four replicate experiments. Large amounts of genetic (between-clone) variation in virulence and transmissibility were observed. Virulence was strongly correlated, both phenotypically and genetically, to population growth rate (parasitaemia) and less strongly correlated to transmissibility. These results provide strong support for the basic tenet of most evolutionary models of parasite virulence, namely, that virulence is a by-product of the parasite's need to replicate fast in order to be transmitted. In the second study, between-host selection for high and low virulence was performed within two parasite clones. Over eleven generations, all the selection lines increased in virulence and transmissibility. Thus, despite artificial between-host selection, parasitic variation within clones coupled with inadvertent within-host selection, allowed the parasite to adapt to a novel host. Together, these studies show that virulence is strongly determined by parasite genetics. A large data set on disease severity from a 3-year longitudinal field study in Sri Lanka was analysed for the effects of host genetic variability, age, immune experience, parasite species (P. falciparum vs. P. vivax), bednet use, sex and other host or environmental factors. The results highlighted the importance of short-term acquired immunity in causing large between-host variation in virulence. This is consistent with the view that parasite variability is responsible for inefficient clinical immunity to malarial disease, although this could not be examined directly and alternative explanations are possible. Two theoretical models incorporating parasite population structure into population genetics were used to predict the probability and rate of evolution of multi-locus drug resistance. All of these studies suggest that parasite genetic variation plays a key role in the evolution of the malaria host-parasite association.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.654346  DOI: Not available
Share: