The DOI matches its Crossref record; 73 of the 73 references it cites were found in a registry or an index.
GENETIC RELATIONSHIPS BETWEEN PARASITE VIRULENCE AND TRANSMISSION IN THE RODENT MALARIA PLASMODIUM CHABAUDI
Abstract
Many parasites evolve to become virulent rather than benign mutualists. One of the major theoretical models of parasite virulence postulates that this is because rapid within-host replication rates are necessary for successful transmission (parasite fitness) and that virulence (damage to the host) is an unavoidable consequence of this rapid replication. Two fundamental assumptions underlying this so-called evolutionary trade-off model have rarely been tested empirically: (1) that higher replication rates lead to higher levels of virulence; and (2) that higher replication rates lead to higher transmission. Both of these relationships must have a genetic basis for this evolutionary hypothesis to be relevant. These assumptions were tested in the rodent malaria parasite, Plasmodium chabaudi, by examining genetic relationships between virulence and transmission traits across a population of eight parasite clones isolated from the wild. Each clone was injected into groups of inbred mice in a controlled laboratory environment, and replication rate (measured by maximum asexual parasitemia), virulence (measured by live-weight loss and degree of anemia in the mouse), and transmission (measured by density of sexual forms, gametocytes, in the blood and proportion of mosquitoes infected after taking a blood-meal from the mouse) were assessed. It was found that clones differed widely in these traits and these clone differences were repeatable over successive blood passages. Virulence traits were strongly phenotypically and genetically (i.e., across clones) correlated to maximum parasitemia thus supporting the first assumption that rapid replication causes higher virulence. Transmission traits were also positively phenotypically and genetically correlated to parasitemia, which supports the second assumption that rapid replication leads to higher transmission. Thus, two assumptions of the parasite-centered trade-off model of the evolution of virulence were shown to be justified in malaria parasites.
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Cited by
Virulence evolution and the trade‐off hypothesis: history, current state of affairs and the future
ALIZON, S., HURFORD, A., MIDEO, N., & VAN BAALEN, M. (2009) · Journal of Evolutionary Biology · doi:10.1111/j.1420-9101.2008.01658.x · Cited by 932
Imperfect vaccines and the evolution of pathogen virulence
Gandon, S., Mackinnon, M. J., Nee, S., & Read, A. F. (2001) · Nature · doi:10.1038/414751a · Cited by 630
Self-citationVirulence and competitive ability in genetically diverse malaria infections
de Roode, J. C., Pansini, R., Cheesman, S. J., Helinski, M. E. H., Huijben, S., Wargo, A. R., Bell, A. S., Chan, B. H. K., Walliker, D., & Read, A. F. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0500078102 · Cited by 422
Self-citationEvolution of virulence in opportunistic pathogens: generalism, plasticity, and control
Brown, S. P., Cornforth, D. M., & Mideo, N. (2012) · Trends in Microbiology · doi:10.1016/j.tim.2012.04.005 · Cited by 416
Metadata
- Authors
- Mackinnon, M. J., & Read, A. F.
- Venue
- Evolution
- Publisher
- Oxford University Press (OUP)
- Published
- 1999-06
- Volume
- 53
- Issue
- 3
- Pages
- 689-703
- ISSN
- 0014-3820 (ISSN-L)
- OpenAlex
- W1974577959
- Cited by
- 302
- References
- 73
- FWCI
- 19.05
- Type
- journal article
- Language
- en
- Open access
- closed
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- Mackinnon, M. J., & Read, A. F. (1999). GENETIC RELATIONSHIPS BETWEEN PARASITE VIRULENCE AND TRANSMISSION IN THE RODENT MALARIA PLASMODIUM CHABAUDI. Evolution. https://doi.org/10.1111/j.1558-5646.1999.tb05364.x
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