In order to spread disease inside the human body, the malaria parasite must evade the human immune system—which it does remarkably well. Now, researchers at Harvard School of Public Health (HSPH) have uncovered details about the mechanism by which the parasite, Plasmodium falciparum, avoids detection—it changes a critical protein on its surface that it uses as one of several molecular “keys” to enter into a new red blood cell. The gene that codes for this protein inside the parasite’s nucleus switches “on and off” at high frequency, which alters its presence on the surface of the parasite.

This process allows the parasite to travel undetected as it moves between red blood cells, which is when it is vulnerable to the immune system. The parasite becomes “itself” again once it is inside a new red blood cell, where it does its dirty work producing a new wave of daughter parasites.

This study, which appears in the December 13, 2012 issue of Cell Host & Microbe, is the first to describe the mechanism of the switching process that occurs in the malaria parasite in such detail, and is a key fundamental biological discovery that could help researchers find new ways of fighting malaria.

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