ArticleMalaria journal2019
Plasticity and genetic variation in traits underpinning asexual replication of the rodent malaria parasite, Plasmodium chabaudi.
Article in Malaria journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Malaria parasites can optimize transmission investment by sensing two within-host cues.PLoS biology · 2025Article
- Virulence is associated with daily rhythms in the within-host replication of the malaria parasiteEvolutionary applications · 2024Article
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- Progeny counter mechanism in malaria parasites is linked to extracellular resources.PLoS pathogens · 2023Article
- Mistimed malaria parasites re-synchronize with host feeding-fasting rhythms by shortening the duration of intra-erythrocytic development.Parasite immunology · 2022Review
- Challenges in forming inferences from limited data: a case study of malaria parasite maturation.Journal of the Royal Society, Interface · 2021Article
- How Many Is Enough? - Challenges of Multinucleated Cell Division in Malaria Parasites.Frontiers in cellular and infection microbiology · 2021Review
- Periodic Parasites and Daily Host Rhythms.Cell host & microbe · 2020Review
- Adaptive phenotypic plasticity in malaria parasites is not constrained by previous responses to environmental change.Evolution, medicine, and public health · 2019Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
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Abstract
backgroundThe ability of malaria (Plasmodium) parasites to adjust investment into sexual transmission stages versus asexually replicating stages is well known, but plasticity in other traits underpinning the replication rate of asexual stages in the blood has received less attention. Such traits include burst size (the number of merozoites produced per schizont), the duration of the asexual cycle, and invasion preference for different ages of red blood cell (RBC).
methodsHere, plasticity [environment (E) effects] and genetic variation [genotype (G) effects] in traits relating to asexual replication rate are examined for 4 genotypes of the rodent malaria parasite Plasmodium chabaudi. An experiment tested whether asexual dynamics differ between parasites infecting control versus anaemic hosts, and whether variation in replication rate can be explained by differences in burst size, asexual cycle, and invasion rates.
resultsThe within-host environment affected each trait to different extents but generally had similar impacts across genotypes. The dynamics of asexual densities exhibited a genotype by environment effect (G×E), in which one of the genotypes increased replication rate more than the others in anaemic hosts. Burst size and cycle duration varied between the genotypes (G), while burst size increased and cycle duration became longer in anaemic hosts (E). Variation in invasion rates of differently aged RBCs was not explained by environmental or genetic effects. Plasticity in burst size and genotype are the only traits making significant contributions to the increase in asexual densities observed in anaemic hosts, together explaining 46.4% of the variation in replication rate.
conclusionsThat host anaemia induces several species of malaria parasites to alter conversion rate is well documented. Here, previously unknown plasticity in other traits underpinning asexual replication is revealed. These findings contribute to mounting evidence that malaria parasites deploy a suite of sophisticated strategies to maximize fitness by coping with, or exploiting the opportunities provided by, the variable within-host conditions experienced during infections. That genetic variation and genotype by environment interactions also shape these traits highlights their evolutionary potential. Asexual replication rate is a major determinant of virulence and so, understanding the evolution of virulence requires knowledge of the ecological (within-host environment) and genetic drivers of variation among parasites.
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