**3.4 Crosstalk between reproduction and immunity**

A relationship between reproductive potential and immune status has been long established. Collectively, these studies suggest a tradeoff between immune activation and egg production, reflected by the identification of follicular atresia and other cell death pathways [71, 72]. Recent advances are now highlighting the role of nutrientsensing pathways and vector immunometabolism [73]. Future studies will provide further insight into how signaling pathways, such as TOR and Insulin pathways, well-known vitellogenic and immune regulators, coordinate energetic balance during infection. Interestingly, previous work using natural combinations of vector-parasite has suggested that coevolution might have minimized the impact of infection [74], possibly by the fact that immune tolerance can induce a less-energetic costly immune response.

Rerouting of yolk components can be used as a nutritional factor for parasite development. Mosquito LP has been incorporated into *Plasmodium* oocyst as a lipid source [75]. While parasite development was accelerated by LP delivery, it did not induce any detectable reproductive cost [76]. Interestingly, mosquito lipids influenced not only total parasite numbers, but also *Plasmodium* sporozoite virulence upon transmission to vertebrate hosts [77]. Similarly, VG is a key component for *Plasmodium* survival. An interplay between YPPs and immune response has been demonstrated. Both LP and VG were shown to reduce the efficiency of the binding of the major parasite-killing TEP1 [78], increasing parasite survival following mosquito infection.
