Plasmodium, the causative agent of malaria, must first infect hepatocytes to 
initiate a mammalian infection. Sporozoites migrate through several hepatocytes, 
by breaching their plasma membranes, before infection is finally established in 
one of them. Here we show that wounding of hepatocytes by sporozoite migration 
induces the secretion of hepatocyte growth factor (HGF), which renders 
hepatocytes susceptible to infection. Infection depends on activation of the HGF 
receptor, MET, by secreted HGF. The malaria parasite exploits MET not as a 
primary binding site, but as a mediator of signals that make the host cell 
susceptible to infection. HGF/MET signaling induces rearrangements of the 
host-cell actin cytoskeleton that are required for the early development of the 
parasites within hepatocytes. Our findings identify HGF and MET as potential 
targets for new approaches to malaria prevention.