The science of epigenetics, or the adaptive changes to DNA in response to life stressors, may have uncovered a new and dynamic antimalarial medication.

Plasmodium falciparum, aka malaria, remains the most deadly infectious disease faced by man, a position it has maintained for thousands of years as it causes hundreds of thousands of deaths annually.

Malaria vaccines, malaria medication, and targeted mosquito treatments have allowed for remarkable progress in the control of this complex, multi-stage parasite, including eradication from countries inside the malaria belt such as Egypt and Cape Verde.

Now though, a multinational team has uncovered a feature in the epigentics of the malaria parasite that controls for a suite of genes. Called a chromatin remodeler, with the abbreviation PfSnf2L, the team believes it could lead to a whole new class of antimalarial medication.

Epigenetics are one of life’s primary drivers of adaptations. They are why human beings who live at high altitude have more oxygenated blood than lowlanders, and why traditional divers and fishermen have greater lung capacities than others of the same ethnic background.

They are in effect, a defense mechanism against stress.

Professor Markus Meißner from LMU Munich and Professor of Biochemistry Gernot Längst from the University of Regensburg led the study team, which found how PfSnf2L is essential for P. falciparum to dynamically adjust gene expression.

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“The unique sequence and functional properties of PfSnf2L led to the identification of a highly specific inhibitor that only kills Plasmodium falciparum,” explains Längst.

“This inhibitor represents a new class of antimalarials, potentially targeting all life cycle stages,” adds Professor Meißner.

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Längst described malaria as one of the most “adaptable diseases we face,” and its potential to develop resistance to existing treatments presents the threat of a severely demoralizing impediment to reducing the malarial burden in world society.

“Future work will focus on testing small molecules that inhibit the parasite’s epigenetic machinery and exploring their effectiveness in preclinical models,” concludes Meißner.