Genetics

Beale, G. H.; CARTER, R.; Walliker, David

doi:10.1016/b978-0-12-407150-6.50012-2

Cited by 53 publications

(49 citation statements)

References 35 publications

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“…If initially rare clones can increase transmission by having a later peak of infection, then why do they not do this in single-clone infections ? Part of the answer may relate to the ecology of P. chabaudi in its natural host, hamnom s rutilans, where it is described as a persistent, chronic infection (Landau & Chabaud 1994) with many hosts harbouring more than one genotype (Beale et al 1978). Mixed infections of the human malaria, P. falciparum, are also common (Creasey et al 1990 ;Day et al 1992).…”

Section: Discussionmentioning

confidence: 99%

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Mixed–genotype infections of malaria parasites: within–host dynamics and transmission success of competing clones

Taylor

Walliker

Read

1997

Proc. R. Soc. Lond. B

114

104

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SUMMARYMixed-genotype infections of microparasites are common, but almost nothing is known about how competitive interactions within hosts affect the subsequent transmission success of individual genotypes. We investigated changes in the composition of mixed-genotype infections of the rodent malaria Plasmodium chabaudi clones CR and ER by monoclonal antibody analysis of the asexual infection in mice, and by PCR amplification of clone-specific alleles in oocysts sampled from mosquitoes which had fed on these mice. Mixed-clone infections were initiated with a 9 : 1 ratio of the two clones, with ER as the minority in the first experiment and CR as the minority in the second experiment.When beginning as the majority, clones achieved parasite densities in mice comparable to those achieved in control (single-clone) infections. When they began as the minority, clones were suppressed to less than 10 % of control parasitaemias during the early part of the infections. However, in mosquitoes, the frequency of the initially rare clone was substantially greater than it was in mice at the start of the infection or four days prior to the feed. In both experiments, the minority clone in the inocula produced as many, or more, oocysts than it did as a single-clone infection. These experiments show that asexual dominance during most of the infection is poorly correlated to transmission probability, and therefore that the assumption that within-host population size correlates to transmission probability may not be warranted. They also raise the fundamental question of why transmission rates of individual genotypes are often higher from mixed than single-clone infections.

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Section: Discussionmentioning

confidence: 99%

“…Two cloned lines of P. chabaudi denoted CR and ER (Beale et al 1978), from the World Health Organisation's Registry of Standard Malaria Parasites, Edinburgh University, were used. The mouse hosts were male C57BL\6J\Ola mice (Harlan, England).…”

Section: Materials and Methods (A) Parasites Mice And Mosquitoesmentioning

confidence: 99%

Mixed–genotype infections of malaria parasites: within–host dynamics and transmission success of competing clones

Taylor

Walliker

Read

1997

Proc. R. Soc. Lond. B

114

104

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“…They were all derived from a single drug-sensitive parasite clone, AS. This was obtained originally from its natural host in the Central African Republic and subsequently passaged through laboratory mice and mosquitoes (3). A pyrimethamine-resistant clone, ASpyr, was derived from AS following selection with pyrimethamine (21).…”

Section: Methodsmentioning

confidence: 99%

Antimalarial Drugs Clear Resistant Parasites from Partially Immune Hosts

Cravo

Culleton

Hunt

et al. 2001

Antimicrob Agents Chemother

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“…Brain involvement similar to cerebral malaria does occur in related rodent species (P. berghei, Rest (1982) which also sequesters in other organs (Alger 1963), and in P. yoelii, Yoeli & Hargreaves 1974;Kaul et al 1994), but this appears to be only after adaptation to the novel host (mice) through serial passage. In addition to its similarities with P. falciparum, the P. chabaudi system is attractive as a model because of the availability of diverse parasite strains cryopreserved shortly after they were derived from the wild (Beale et al 1978), the availability of host genotypes with well-characterized genetics, the ability to measure virulence, multiplication rate, gametocyte production, transmission to mosquitoes, cytoadherence and antigenic variation in vivo, and the ability to manipulate immunity and other factors that moderate virulence.…”

Section: Plasmodium Chabaudi As a Model For Virulence Evolutionmentioning

confidence: 99%

Virulence in malaria: an evolutionary viewpoint

Mackinnon

Read

2004

Phil. Trans. R. Soc. Lond. B

228

205

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Malaria parasites cause much morbidity and mortality to their human hosts. From our evolutionary perspective, this is because virulence is positively associated with parasite transmission rate. Natural selection therefore drives virulence upwards, but only to the point where the cost to transmission caused by host death begins to outweigh the transmission benefits. In this review, we summarize data from the laboratory rodent malaria model, Plasmodium chabaudi, and field data on the human malaria parasite, P. falciparum, in relation to this virulence trade-off hypothesis. The data from both species show strong positive correlations between asexual multiplication, transmission rate, infection length, morbidity and mortality, and therefore support the underlying assumptions of the hypothesis. Moreover, the P. falciparum data show that expected total lifetime transmission of the parasite is maximized in young children in whom the fitness cost of host mortality balances the fitness benefits of higher transmission rates and slower clearance rates, thus exhibiting the hypothesized virulence trade-off. This evolutionary explanation of virulence appears to accord well with the clinical and molecular explanations of pathogenesis that involve cytoadherence, red cell invasion and immune evasion, although direct evidence of the fitness advantages of these mechanisms is scarce. One implication of this evolutionary view of virulence is that parasite populations are expected to evolve new levels of virulence in response to medical interventions such as vaccines and drugs.

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Genetics

Cited by 53 publications

References 35 publications

Mixed–genotype infections of malaria parasites: within–host dynamics and transmission success of competing clones

Mixed–genotype infections of malaria parasites: within–host dynamics and transmission success of competing clones

Antimalarial Drugs Clear Resistant Parasites from Partially Immune Hosts

Virulence in malaria: an evolutionary viewpoint

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