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How does natural selection solve the trade-off malaria parasites face between replication within a host and transmission from it?
Like many pathogens, malaria parasites, clonally proliferate within a host, but then use a different life stage for transmission. These transmission stages (gametocytes) are incapable of further replication in the verterbrate host. Gametocytes are thus costly in terms of within-host fitness(especially given the compounding affect of preventing clonal replication) but essential for between host fitness. This is the growth versus reproduction trade-off faced by most organisms. What pattern of gametocyte production should be favoured by natural selection? How might interventions like vaccination or bednets alter optimal life history strategies?
Our attack on this problem is two-fold.
- The development of mathematical models to predict patterns of gametocyte production expected under different hypotheses.
- Estimating the patterns of gametocyte conversion seen in rodent malaria infections.
Developing the models is relatively straight forward, and there are some interesting theoretical possibilities. For instance, the parasites might be exercising reproductive restraint: producing fewer than maximal gametocytes in order to keep them below immune detection levels, or using asexual parasites to distract the immune system from the gametocytes. Alternatively, patterns of gametocytogenesis may in fact maximise total gametocyte numbers in the face of declining reproductive value as hosts become immune.
Testing these ideas is the problem. It is turning out to be very difficult to get estimates of gametocyte conversion we believe. But could be worse. We could be trying to do it on P. falciparum
Group members involved: Lucy Crooks