The cost of immunity in the yellow fever mosquito, Aedes aegypti depends on immune activation

Although host immunity offers the obvious benefit of reducing parasite infection, it is often traded-off with other fitness components. We investigated whether the cost of an immune response in the yellow fever mosquito, Aedes aegypti, is modulated by the antigen that activates the melanization immune response. Thus, one of three different novel antigens were injected into the mosquito's thorax--either a glass bead, a negatively charged (C-25) Sephadex bead, or a neutral (G-25) Sephadex bead--and fecundity and bead melanization were observed. Glass beads are immunologically inert and were therefore used as an inoculation control. The fecundity of mosquitoes inoculated with these beads did not differ from the fecundity of mosquitoes that did not melanize negatively charged or neutral beads. The ability of A. aegypti to melanize negatively charged Sephadex beads was associated with reduced fecundity, showing a clear cost of immunity. In contrast, melanization of the neutral beads was quite strong but had no effect on fecundity. Thus, the cost of what appeared to be the same immune response--melanization of a bead--depended on the type of bead that stimulated the immune system. Such differences might help to explain variation of immune efficacy against different parasites in natural populations.     

Direct and indirect immunosuppression by a malaria parasite in its mosquito vector

Malaria parasites develop as oocysts within the haemocoel of their mosquito vector during a period that is longer than the average lifespan of many of their vectors. How can they escape from the mosquito''s immune responses during their long development? Whereas older oocysts might camouflage themselves by incorporating mosquito-derived proteins into their surface capsule, younger stages are susceptible to the mosquito''s immune response and must rely on other methods of immune evasion. We show that the malaria parasite Plasmodium gallinaceum suppresses the encapsulation immune response of its mosquito vector, Aedes aegypti, and in particular that the parasite uses both an indirect and a direct strategy for immunosuppression. Thus, when we fed mosquitoes with the plasma of infected chickens, the efficacy of the mosquitoes to encapsulate negatively charged Sephadex beads was considerably reduced, whether the parasite was present in the blood meal or not. In addition, zygotes that were created ex vivo and added to the blood of uninfected chickens reduced the efficacy of the encapsulation response. As dead zygotes had no effect on encapsulation, this result demonstrates active suppression of the mosquito''s immune response by malaria parasites.     

The spatial spread of altruism versus the evolutionary response of egoists

Several recent models have shown that altruism can spread in viscous populations, i.e. in spatially structured populations within which individuals interact only with their immediate neighbours and disperse only over short distances. I first confirm this result with an individual-based model of a viscous population, where an individual can vary its level of investment into a behaviour that is beneficial to its neighbours but costly to itself. Two distinct classes of individuals emerge: egoists with no or very little investment into altruism, and altruists with a high level of investment; intermediate levels of altruism are not maintained. I then extend the model to investigate the consequences of letting interaction and dispersal distances evolve along with altruism. Altruists maintain short distances, while the egoists respond to the spread of altruism by increasing their interaction and dispersal distances. This allows the egoistic individuals to be maintained in the population at a high frequency. Furthermore, the coevolution of investment into altruism and interaction distance can lead to a stable spatial pattern, where stripes of altruists (with local interactions) alternate with stripes of egoists (with far-reaching interactions). Perhaps most importantly, this approach shows that the ease with which altruism spreads in viscous populations is maintained despite countermeasures evolved by egoists.     

Coping with change

Extreme Environmental Change and Evolution by A.A. Hoffmann and P.A. Parsons Cambridge University Press, 1997. ￡55.00/$74.95 hbk, ￡19.95/$29.95 pbk (xii+259 pages) ISBN 0 521 44107 2/0 521 44659 7.     

Effects of Age and Larval Nutrition on Phenotypic Expression of Insecticide-Resistance in Anopheles Mosquitoes

Insecticide-resistance threatens the control of mosquito-borne diseases like malaria or dengue fever. To ensure sustainable vector control we need a full understanding of the factors driving the evolution of resistance. We test the hypothesis that the expression of insecticide-resistance depends on the available resources by rearing genetically DDT-resistant and sensitive larvae of Anopheles mosquitoes at three diet regimes, which correspond to 40%, 70% and 100% of the normal diet and exposing the adult females to DDT 5, 10 and 15 days after emergence. In both colonies post-exposure survival decreased with age at exposure. Additionally, the food levels and DDT-resistance were positively correlated in both colonies, although only in the DDT-resistant one was this relationship statistically significant. The impact of larval diet was smaller than the effect of age at exposure. We discuss our results and explain the implication of this study to resistance monitoring for public health and vector management.     

Epidemiological evidence for an association between chloroquine resistance of Plasmodium falciparum and its immunological properties

The appearance of chloroquine-resistant genotypes o f Plasmodium falciparum has thwarted the goal of global eradication of malaria. Although much effort has been put into understanding the molecular mechanisms of chloroquine resistance, many questions about its distribution remain open: Why, some 30 years after the emergence o f chloroquine resistance, have resistant genotypes not taken over the population? Why have many parasites remained sensitive? Why, after its first appearance in Africa, has chloroquine resistance spread so rapidly through sub-Saharan Africa? In this paper Jacob Koella reviews epidemiological data that suggest that an answer to these questions may involve an association between chloroquine resistance and immunological properties o f malaria parasites.     

Costs and benefits of resistance against antimalarial drugs

Recent experiments have suggested that resistance to antimalarial drugs, in particular chloroquine, is associated with increased transmission. However, epidemiological patterns suggest the opposite: ie. that resistance should be associated with a transmission cost. Here, Jacob Koella reviews the evidence for either a cost or a benefit of chloroquine resistance and proposes ideas from population and evolutionary biology that might explain the apparent contradiction between experimental and epidemiological evidence.     

A correlated response of a parasite’s virulence and life cycle to selection on its host’s life history

We demonstrate a correlated response of the virulence and the mode of transmission of the microsporidian parasite Edhazardia aedis to selection on the age at pupation of its host, the mosquito Aedes aegypti. We selected three lines of mosquitoes each for early or late pupation and exposed the larvae after zero, two and four generations of selection to a low and a high concentration of the parasite’s spores. Before selection the parasites induced a similar level of mortality in the six lines; after four generations of selection mortality was higher in the mosquitoes selected for late pupation than in those selected for early pupation. Overall, parasite-induced mortality was positively correlated with the mean age at pupation of the matching uninfected line. When they died, mosquitoes selected for early pupation harboured mostly binucleate spores, which are responsible for vertical transmission. Mosquitoes selected for late pupation were more likely to harbour uninucleate spores, which are responsible for horizontal transmission. The parasite enhanced this tendency for horizontal transmission by prolonging the larval period in the lines selected for late pupation, but not in the ones selected for early pupation. These results suggest that the genetic basis of the mosquito’s age at pupation helps to determine the parasite’s mode of transmission: parasites in rapidly developing mosquitoes are benign and transmit vertically, while parasites in slowly developing mosquitoes are virulent and transmit horizontally. Thus, as the host’s life history evolves, the parasite’s performance changes, because the host’s evolution changes the environment in which the parasite develops.