Scientists have discovered the genetic mechanism that causes some people to develop only mild cases of malaria, a mosquito borne illness that usually causes extremely high fevers and occasionally death.  VOA's Jessica Berman reports the discovery could change the way traditional malaria drugs are used.

Malaria infects approximately 350 million people each year, many develop headache, nausea, chills and vomiting.  But the parasitic disease is often deadly, and each year is blamed for the deaths of more than one million people, mostly children in sub-Saharan Africa. 

But not everyone who is bitten by an infected mosquito develops life-threatening complications.  Some people experience malaria as little more than a mild case of the flu.

University of Toronto Professor of Medicine Kevin Kain says those who have sickle cell anemia or those who have inherited a single gene for sickle cell, but do not actually have the disease, are protected from malaria. 

Dr. Kain says it has to do with a deficiency in an enzyme called pyruvate kinase, which people with sickle anemia and some other red-blood-cell illnesses, known as PKD disorders, have in common.

"All of these disorders, which seem quite different, seem to have a common theme in how they prevent or at least protect against severe malaria and fatal malaria," he said.  "They all seem to help your innate immune system clear malaria better than you would normally."

Dr. Kain says approximately one in 20,000 people is deficient in pyruvate kinase.  The experts say it appears the malaria parasite needs the pathway produced by the pyruvate kinase enzyme in blood to thrive after infecting its human host.

To prove that a deficiency of the enzyme might be protective against malaria, Dr. Kain and colleagues at the University of Toronto took blood samples from several PKD patients and found they could not sustain an infection with the malaria parasites, which easily infected blood samples from healthy participants.

Dr. Kain says the finding could lead to new and better drugs that specifically target malaria at the molecular level, instead of bombarding the parasite with drugs that over time have become ineffective.

"So [we can] change our model from just trying to kill malaria parasites to thinking also of how we can enhance these protective pathways that, evolution is kind of teaching us, [may] work," he added.

Kain notes that people who have a disorder like sickle cell have inherited a defective copy of the pyruvate kinase gene from each parent and are very sick.  But he says it may be possible to target a single gene for a malaria drug without harm.

The study on malaria is published in this week's New England Journal of Medicine.