Malaria transmission between human and mosquito depends on the number of male and female gametocytes in the blood.

A mathematical model of blood-stage infection with Plasmodium falciparum malaria capturing the sexual stage of the parasite life-cycle is validated against human data, providing new insight into human-to-mosquito transmission.

Controlled human malaria infection model allows the study of gametocyte biology and dynamics providing novel insights and tools in malaria transmission and elimination efforts.

The controlled infection of volunteers with Plasmodium falciparum parasites could provide a platform to evaluate new drugs and vaccines aimed at blocking malaria transmission.

Treatment of malaria parasites with the frontline antimalarial drug artemisinin can increase the proportion of parasites that convert into transmission forms.

Multiple steps of the atypical cell cycles underlying Plasmodium gametogony are controlled by a divergent cyclin/cyclin-dependent complex.

Plasmodium parasite transcription shifts dramatically along asexual development, and transmission stages variably express important immune evasion genes, suggesting much interesting biology has until now been hidden by bulk analyses.

A surface protein triggers intra-oocyst motility of Plasmodium sporozoites to ensure parasite egress from oocysts.

Lower malaria prevalence in females does not appear to be due to lower rates of infection but rather due to faster clearance of asymptomatic infections.

Exchange of the I domain in the Plasmodium surface protein TRAP against evolutionary distant I domains rescues infectivity of sporozoites.