1. Immunity Promotes Virulence Evolution in a Malaria Model
Abstract
“Evolutionary models predict that host immunity will shape the evolution of parasite virulence. While some assumptions of these models have been tested, the actual evolutionary outcome of immune selection on virulence has not. Using the mouse malaria model, Plasmodium chabaudi, we experimentally tested whether immune pressure promotes the evolution of more virulent pathogens by evolving parasite lines in immunized and nonimmunized (‘‘naı¨ve’’) mice using serial passage. We found that parasite lines evolved in immunized mice became more virulent to both naı¨ve and immune mice than lines evolved in naı¨ve mice. When these evolved lines were transmitted through mosquitoes, there was a general reduction in virulence across all lines. However, the immune-selected lines remained more virulent to naı¨ve mice than the naı¨ve-selected lines, though not to immunized mice. Thus, immune selection accelerated the rate of virulence evolution, rendering parasites more dangerous to naı¨ve hosts. These results argue for further consideration of the evolutionary consequences for pathogen virulence of vaccination.”
Links
http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0020230
Citation
Mackinnon, Margaret J., and Andrew F. Read. "Immunity Promotes Virulence Evolution in a Malaria Model." PLoS Biology 2.9 (2004)
“Evolutionary models predict that host immunity will shape the evolution of parasite virulence. While some assumptions of these models have been tested, the actual evolutionary outcome of immune selection on virulence has not. Using the mouse malaria model, Plasmodium chabaudi, we experimentally tested whether immune pressure promotes the evolution of more virulent pathogens by evolving parasite lines in immunized and nonimmunized (‘‘naı¨ve’’) mice using serial passage. We found that parasite lines evolved in immunized mice became more virulent to both naı¨ve and immune mice than lines evolved in naı¨ve mice. When these evolved lines were transmitted through mosquitoes, there was a general reduction in virulence across all lines. However, the immune-selected lines remained more virulent to naı¨ve mice than the naı¨ve-selected lines, though not to immunized mice. Thus, immune selection accelerated the rate of virulence evolution, rendering parasites more dangerous to naı¨ve hosts. These results argue for further consideration of the evolutionary consequences for pathogen virulence of vaccination.”
Links
http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0020230
Citation
Mackinnon, Margaret J., and Andrew F. Read. "Immunity Promotes Virulence Evolution in a Malaria Model." PLoS Biology 2.9 (2004)
2. Imperfect vaccination: some epidemiological and evolutionary consequences
Abstract
“An aim of some vaccination programmes is to reduce the prevalence of an infectious disease and ultimately to eradicate it. We show that eradication success depends on the type of vaccine as well as on the vaccination coverage. Vaccines that reduce the parasite within-host growth rate select for higher parasite virulence and this evolution may both increase the prevalence of the disease and prevent disease eradication. By contrast, vaccines that reduce the probability of infection select against virulence and may lead more easily to eradication. In some cases, epidemiological feedback on parasite evolution yields an evolutionary bistable situation where, for intermediate vaccination coverage, parasites can evolve towards either high or low virulence, depending on the initial conditions. These results have practical implications for the design and use of imperfect vaccines in public- and animal-health programmes”
Links
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1691350/
Citations
Gandon, S., M. Mackinnon, S. Nee, and A. Read. "Imperfect Vaccination: Some Epidemiological and Evolutionary Consequences." Proceedings of the Royal Society B: Biological Sciences 270.1520 (2003): 1129-136.
“An aim of some vaccination programmes is to reduce the prevalence of an infectious disease and ultimately to eradicate it. We show that eradication success depends on the type of vaccine as well as on the vaccination coverage. Vaccines that reduce the parasite within-host growth rate select for higher parasite virulence and this evolution may both increase the prevalence of the disease and prevent disease eradication. By contrast, vaccines that reduce the probability of infection select against virulence and may lead more easily to eradication. In some cases, epidemiological feedback on parasite evolution yields an evolutionary bistable situation where, for intermediate vaccination coverage, parasites can evolve towards either high or low virulence, depending on the initial conditions. These results have practical implications for the design and use of imperfect vaccines in public- and animal-health programmes”
Links
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1691350/
Citations
Gandon, S., M. Mackinnon, S. Nee, and A. Read. "Imperfect Vaccination: Some Epidemiological and Evolutionary Consequences." Proceedings of the Royal Society B: Biological Sciences 270.1520 (2003): 1129-136.
3. Imperfect Vaccines And The Evolution Of Pathogens Causing Acute Infections In Vertebrates
Abstract
“A study by Gandon et al. (2001) considered the potential ways pathogens may evolve in response to vaccination with imperfect vaccines. In this paper, by focusing on acute infections of vertebrate hosts, we examine whether imperfect vaccines that do not completely block a pathogen's replication (antigrowth) or transmission (an- titransmission) may lead to evolution of more or less virulent pathogen strains. To address this question, we use models of the within-host dynamics of the pathogen and the host's immune responses. One advantage of the use of this within-host approach is that vaccination can be easily incorporated in the models and the trade-offs between pathogen transmissibility, host recovery, and virulence that drive evolution of pathogens in these models can be easily estimated. We find that the use of either antigrowth or antitransmission vaccines leads to the evolution of pathogens with an increased within-host growth rate; infection of unvaccinated hosts with such evolved pathogens results in high host mortality and low pathogen transmission. Vaccination of only a fraction of hosts with antigrowth vaccines may prevent pathogens from evolving high virulence due to pathogen adaptation to unvaccinated hosts and thus protection of vaccinated hosts from pathogen-induced disease. In contrast, antitransmission vaccines may be beneficial only if they are effective enough to cause pathogen extinction. Our results suggest that particular mechanisms of action of vaccines and their efficacy are crucial in predicting longterm evolutionary consequences of the use of imperfect vaccines.”
Links
https://www.ncbi.nlm.nih.gov/pubmed/16817536
Citations
Ganusov, Vitaly V., and Rustom Antia. "Imperfect Vaccines And The Evolution Of Pathogens Causing Acute Infections In Vertebrates." Evolution 60.5 (2006): 957.
“A study by Gandon et al. (2001) considered the potential ways pathogens may evolve in response to vaccination with imperfect vaccines. In this paper, by focusing on acute infections of vertebrate hosts, we examine whether imperfect vaccines that do not completely block a pathogen's replication (antigrowth) or transmission (an- titransmission) may lead to evolution of more or less virulent pathogen strains. To address this question, we use models of the within-host dynamics of the pathogen and the host's immune responses. One advantage of the use of this within-host approach is that vaccination can be easily incorporated in the models and the trade-offs between pathogen transmissibility, host recovery, and virulence that drive evolution of pathogens in these models can be easily estimated. We find that the use of either antigrowth or antitransmission vaccines leads to the evolution of pathogens with an increased within-host growth rate; infection of unvaccinated hosts with such evolved pathogens results in high host mortality and low pathogen transmission. Vaccination of only a fraction of hosts with antigrowth vaccines may prevent pathogens from evolving high virulence due to pathogen adaptation to unvaccinated hosts and thus protection of vaccinated hosts from pathogen-induced disease. In contrast, antitransmission vaccines may be beneficial only if they are effective enough to cause pathogen extinction. Our results suggest that particular mechanisms of action of vaccines and their efficacy are crucial in predicting longterm evolutionary consequences of the use of imperfect vaccines.”
Links
https://www.ncbi.nlm.nih.gov/pubmed/16817536
Citations
Ganusov, Vitaly V., and Rustom Antia. "Imperfect Vaccines And The Evolution Of Pathogens Causing Acute Infections In Vertebrates." Evolution 60.5 (2006): 957.
4. Virulence in malaria: an evolutionary viewpoint
Abstract
“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.”
Links
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1693375/
Citations
Mackinnon, M. J., and A. F. Read. "Virulence in Malaria: An Evolutionary Viewpoint." Philosophical Transactions of the Royal Society B: Biological Sciences 359.1446 (2004): 965-86.
“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.”
Links
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1693375/
Citations
Mackinnon, M. J., and A. F. Read. "Virulence in Malaria: An Evolutionary Viewpoint." Philosophical Transactions of the Royal Society B: Biological Sciences 359.1446 (2004): 965-86.