Plasmodium cross-stage interplay dictates malaria outcome

If you are interested in joining the seminar, please contact: vseminars@mpiib-berlin.mpg.de

Once registered, you will receive a zoom conference link 30 mins before the talk starts - please sign in using your full name.

Talk abstract:

Using rodent models of Plasmodium infection, we show that integration of signals from the two stages of parasite development within the mammalian host dictates survival or death. This dichotomy relies on liver stage-dependent activation of Vγ4+ γδ T cells, which exhibit distinct cytokine profiles selectively sustained by different blood stage parasite loads. Our findings challenge the current understanding on the mechanisms underlying the pathophysiology of malaria infections, repositioning Plasmodium liver-stage infection from a transient phase of parasite expansion into a critical contributor for the clinical outcome of infection.

Most of the research efforts in the malaria field have focused on the clinically relevant blood-stage of infection, even though the successful establishment of infection depends on Plasmodium intra-hepatic development. The fact that the clinical manifestations of malaria only arise during the blood stage of infection has cemented the perception that liver infection does not influence the ensuing pathology.

Malaria imposes an immense public health and economic burden on large parts of the world. Plasmodium, the causative agent of malaria, has a complex live cycle that in the vertebrate host encompasses two distinct stages, i.e., the clinically silent pre-erythrocytic stage where the parasite grows and replicates within the hepatocyte and the blood-stage of infection, associated with the establishment of disease and all its complications.