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Throughout infections, malaria parasites show considerable variation in their allocation of resources to male and female gametocytes. Furthermore, malaria parasites facultatively alter their investment in gametocytes and their sex ratio in response to changes in their within-host environment. Such variable sex ratios within infections are not predicted by classical LMC theory. Despite the potential for medical interventions that disrupt sexual reproduction and block transmission, we understand relatively little about why malaria and related protozoan parasites vary their reproductive behaviors throughout infections. One possible explanation is that parasites adjust their sex ratio strategy to compensate for reductions in their fertilisation success ('fertility insurance'). Theory has shown that when there is a risk that all the female gametocytes in a blood meal may not be fertilised, parasites should respond by either changing their sex ratio (less female-biased), or by increasing the number of gametocytes they produce. Fertilisation success could be reduced when hosts are anaemic, or by the variety of immune factors that appear in the host's circulation, or a combination of these. If these factors vary throughout infections, then the importance of a fertility insurance strategy will also vary. Fertility insurance theory incorporates LMC and predicts lower female bias, for a given inbreeding rate, than classical LMC theory.

The in-host environment experienced by malaria parasites is predicted to determine when fertility insurance is important. Transmission-blocking immunity (TBI) is predicted to influence the production of functional male gametes and host anaemia is expected to influence the number of gametocytes whose gametes can interact in a blood meal. The existence of TBI has been well documented and various antibodies, white blood cells and factors such as nitric oxide have all been implicated in reducing transmission. TBI could reduce fertilisation success in a number of ways, including agglutinating male gametes and reducing their motility/viability. Severe anaemia occurs during infections and blood meals from sick hosts may only contain a small number of gametocytes. When male gamete production is low and few gametocytes are able to interact in a blood meal, parasites are expected to alter their sex ratio by increasing their investment in male gametocytes or gametocytes, to ensure that they have produced enough males to fertilise their females. Levels of TBI and anaemia vary throughout infections, which leads to the prediction that parasite responses to fertility insurance will co-vary with TBI and anaemia. This is supported by observations that malaria parasites change either their investment in gametocytes or sex ratio in response to artificial manipulations of host anaemia. Furthermore, these parasites had a lower fertilisation success compared to parasites in control infections. We predict that when fertility insurance is important and preferred red cells are abundant, parasites have enough resources to increase investment in gametocytes, and sex ratio will reflect their inbreeding rate. Conversely, if preferred red cells are scarce, parasites cannot afford to increase investment in gametocytes but can only alter their sex ratio - in this case they should produce more males relative to females. This is supported by data showing that rodent malaria parasites have different response to experimentally induced anaemia: P. chabaudi can use reticulocytes and increases investment in gametocytes but P. vinckei cannot use reticulocytes and increases investment in males.

Back to research outline or more on malaria parasite reproductive strategies, explaining facultative reproductive strategies or reproductive strategies in mixed-species infections.

SARAH REECE