A new study uncovers an important step in the malaria parasite’s ability to gain a foothold in the human liver, where it replicates before spreading to the bloodstream. The discovery could lead to new ways to block parasite infection.

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Scientists (here dissecting malaria-carrying mosquitoes) have uncovered a key step that allows malaria parasites to invade liver cells in humans.
Image credit: Center for Infectious Disease Research

The study, from the Center for Infectious Disease Research (CIDR) in Seattle, WA, is published in the journal Science.

The more we know about the malaria parasite’s complex lifecycle, the greater our ability to fight a disease that kills half a million people a year, mostly children in the African Region.

The malaria parasite requires two hosts to complete its lifecycle: humans and female Anopheles mosquitoes. The parasite enters the human body through the bite of the female mosquito when she takes a blood meal.

When it enters a human host, the malaria parasite targets the liver, where it invades liver cells and uses them to grow and multiply before moving onto another stage of growth in red blood cells.

It is the blood stage of the lifecycle that causes the potentially fatal symptoms of malaria and also allows it to spread to other hosts via the bite of mosquitoes.

The new study uncovers a critical step in the liver-invasion stage of the malaria parasite. Stopping the lifecycle at this stage might not only prevent full-blown disease symptoms in the infected person, but it could also help stop malaria spread in the population.

When it enters liver cells, the malaria parasite occupies replication compartments called “parasitophorous vacuoles” where it carries out the task of multiplying itself.

In the new study, the team found that the malaria parasite prefers to enter liver cells expressing the EphA2 receptor, because this allows the parasite to establish in vacuoles and set about replicating itself.

They showed that the parasites readily invaded liver cells that highly expressed EphA2, but in mice lacking the receptor, there was no liver invasion.

And, in a final step, the team showed that the parasite protein P36 is the “key” that “unlocks” the EphA2 receptor to allow entry into the liver cell.

Lead author Alexis Kaushansky, an assistant professor at CIDR, says:

This discovery is significant because it reveals a vital interaction between the malaria parasite and the person it infects. Before, we knew little about that interaction. The molecular details of our discovery will facilitate the design of new drugs and new vaccines.”

Medical News Today recently learned about another exciting development in the fight against malaria, where scientists at the University of California created a strain of gene-edited mosquitoes that is capable of rapidly spreading malaria-resistant genes into a mosquito population through its offspring.