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51.
It has often been suggested that vector-borne parasites alter their vector''s feeding behaviour to increase their transmission, but these claims are often based on laboratory studies and lack rigorous testing in a natural situation. We show in this field study that the malaria parasite, Plasmodium falciparum, alters the blood-feeding behaviour of its mosquito vector, Anopheles gambiae s.l., in two ways. First, mosquitoes infected with sporozoited, the parasite stage that is transmitted from the mosquito to a human, took up larger blood meals than uninfected mosquitoes. Whereas 72% of the uninfected mosquitoes had obtained a full blood meal, 82% of the infected ones had engorged fully. Second, mosquitoes harbouring sporozoites were more likely to bite several people per night. Twenty-two per cent of the infected mosquitoes, but only 10% of the uninfected mosquitoes, contained blood from at least two people. We conclude that the observed changes in blood-feeding behaviour allow the parasite to spread more rapidly among human hosts, and thus confirm that the parasite manipulates the mosquito to increase its own transmission.  相似文献   
52.
Despite considerable theoretical advances in the evolutionary biology of host–parasite systems, our knowledge of host–parasite coevolution in natural systems is often limited. Among the reasons for the lag of experimental insight behind theory is that the parasite's virulence is not a simple trait that is controlled by the parasite's genes. Rather, virulence can be expressed in several traits due to the subtle interactions between the host and the parasite. Furthermore, the host might evolve tolerance to the parasite if there is sufficient genetic variance to reduce the detrimental effect of the parasite on these traits. We studied the traits underlying virulence and the genetic potential to evolve tolerance to infection in the host–parasite system Aedes aegypti – Brachiola algerae . We reared the mosquitoes in a half-sib design, exposed half of the individuals in each full-sib family to the parasite and measured several life history traits – juvenile mortality, age at pupation and adult size – of infected and uninfected individuals. Virulence was due in large part to a delay of the mosquito's age at pupation by about 10%. Although this imposes strong selection pressure on the mosquito to resist the parasite, all of the mosquitoes were infected, implying a lack of resistance. Furthermore, although additive genetic variance was present for other traits, we found no indication of additive genetic variation for the age at pupation, nor for the delay of pupation due to infection, implying no potential for the evolution of tolerance. Overall, the results suggest that in this host–parasite system, the host has little evolutionary control over the expression of the parasite's virulence.  相似文献   
53.
To investigate the evolutionary cost of an immune response, we selected six lines of the mosquito Aedes aegypti for earlier or later pupation and measured the extent to which this selection procedure changed the mosquito's ability to encapsulate and melanize a negatively charged Sephadex bead. After 10 generations of selection, the age at pupation in the two selection regimes differed by about 0.7 days, accompanied by an increase of wing length of the mosquitoes selected for late pupation. Among the mosquitoes that had been selected for early pupation, only 6% had strongly or completely melanized the bead, while among the individuals that had been selected for late pupation, 32% had melanized the bead. Thus, our results suggest a genetic correlation between age at pupation and immunocompetence. As a consequence, mosquitoes that respond to increased intense parasite pressure with more effective immunity are predicted to pay for the increased defense with slower development.  相似文献   
54.
Concurrent evolution of resistance and tolerance to pathogens   总被引:1,自引:0,他引:1  
Recent experiments on plant defenses against pathogens or herbivores have shown various patterns of the association between resistance, which reduces the probability of being infected or attacked, and tolerance, which reduces the loss of fitness caused by the infection or attack. Our study describes the simultaneous evolution of these two strategies of defense in a population of hosts submitted to a pathogen. We extended previous approaches by assuming that the two traits are independent (e.g., determined by two unlinked genes), by modeling different shapes of the costs of defenses, and by taking into account the demographic and epidemiological dynamics of the system. We provide novel predictions on the variability and the evolution of defenses. First, resistance and tolerance do not necessarily exclude each other; second, they should respond in different ways to changes in parameters that affect the epidemiology or the relative costs and benefits of defenses; and third, when comparing investments in defenses among different environments, the apparent associations among resistance, tolerance, and fecundity in the absence of parasites can lead to the false conclusion that only one defense trait is costly. The latter result emphasizes the problems of estimating trade-offs and costs among natural populations without knowledge of the underlying mechanisms.  相似文献   
55.
Do malaria parasites enhance the attractiveness of humans to the parasite's vector? As such manipulation would have important implications for the epidemiology of the disease, the question has been debated for many years. To investigate the issue in a semi-natural situation, we assayed the attractiveness of 12 groups of three western Kenyan children to the main African malaria vector, the mosquito Anopheles gambiae. In each group, one child was uninfected, one was naturally infected with the asexual (non-infective) stage of Plasmodium falciparum, and one harboured the parasite's gametocytes (the stage transmissible to mosquitoes). The children harbouring gametocytes attracted about twice as many mosquitoes as the two other classes of children. In a second assay of the same children, when the parasites had been cleared with anti-malarial treatment, the attractiveness was similar between the three classes of children. In particular, the children who had previously harboured gametocytes, but had now cleared the parasite, were not more attractive than other children. This ruled out the possibility of a bias due to differential intrinsic attractiveness of the children to mosquitoes and strongly suggests that gametocytes increase the attractiveness of the children.  相似文献   
56.
Coevolutionary interactions between host and parasite genotypes   总被引:5,自引:0,他引:5  
More than 20 years after Dawkins introduced the concept of "extended phenotype" (i.e. phenotypes of hosts and parasites result from interactions between the two genomes) and although this idea has now reached contemporary textbooks of evolutionary biology, most studies of the evolution of host-parasite systems still focus solely on either the host or the parasite, neglecting the role of the other partner. It is important to consider that host and parasite genotypes share control of the epidemiological parameters of their relationship. Moreover, not only the traits of the infection but also the genetic correlations among these and other traits that determine fitness might be controlled by interactions between host and parasite genotypes.  相似文献   
57.
The genetic basis of a host's resistance to parasites has important epidemiological and evolutionary consequences. Understanding this genetic basis can be complicated by non-genetic factors, such as environmental quality, which may influence the expression of genetic resistance and profoundly alter patterns of disease and the host's response to selection. In particular, understanding the environmental influence on the genetic resistance of mosquitoes to malaria gives valuable knowledge concerning the use of malaria-resistant transgenic mosquitoes as a measure of malaria control. We made a step towards this understanding by challenging eight isofemale lines of the malaria vector Anopheles stephensi with the rodent malaria parasite Plasmodium yoelii yoelii and by feeding the mosquitoes with different concentrations of glucose. The isofemale lines differed in infection loads (the numbers of oocysts), corroborating earlier studies showing a genetic basis of resistance. In contrast, the proportion of infected mosquitoes did not differ among lines, suggesting that the genetic component underlying infection load differs from the genetic component underlying infection rate. In addition, the mean infection load and, in particular, its heritable variation in mosquitoes depended on the concentration of glucose, which suggests that the environment affects the expression and the evolution of the mosquitoes' resistance in nature. We found no evidence of genotype-by-environment interactions, i.e. the lines responded similarly to environmental variation. Overall, these results indicate that environmental variation can significantly reduce the importance of genes in determining the resistance of mosquitoes to malaria infection.  相似文献   
58.
This paper describes how a parasite with distinct stages for replication within its host and for transmission among hosts should schedule the production of the two stages so that it achieves maximal transmission. A mathematical model of the within-host dynamics of a parasite and of its interactions with the immune response predicts that the optimal pattern of investment depends largely on the relationships between the growth rate of the parasite, the rate of increase of immunity against the parasite, and parasite-induced mortality of the host. We consider first a parasite with a constant, time-independent level of investment in transmission. If such a parasite grows rapidly and can therefore reach a density that kills the host before it is cleared by the immune response, it can achieve maximal transmission by producing transmission stages, and thus reducing its effective growth rate, to the extent that its peak density is just below the lethal density. This leads to the prediction that investment in transmission should be positively correlated with growth rate. In contrast, if the parasite grows more slowly and is cleared by the immune system before it can reach lethal density, the level of investment should be negatively correlated with growth rate. If a parasite can vary its investment into transmission during the course of infection, it should delay investment into transmission until it reaches lethal density or until shortly before it is cleared by the host′s immune system. If a parasite grows slowly in comparison with immunity, the optimal pattern of investment is a bang-bang pattern: the investment switches from total production of the replication stage to total production of the transmission stage shortly before the parasite is cleared by the immune response. If a parasite grows much more rapidly than immunity, the parasite initially replicates up to lethal density without producing any transmission stages, then produces transmission stages at the rate that reduces its effective growth rate to zero and thus allows it to be maintained at lethal density, and finally switches to complete investment into transmission stages shortly before it is cleared by the immune system  相似文献   
59.
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