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Genetic studies shed light on the malaria parasite's origins and drug resistance

Researchers at the National Institutes of Health (NIH) report mining the genome of the malaria parasite has uncovered new data showing the parasite is genetically more diverse and much older -- at least 100,000 years old -- than some scientists have thought. The new information suggests creating vaccines to control the deadly disease poses a greater challenge than some may have imagined.

In a second paper, the NIH-led group also found that parasites resistant to chloroquine, a former mainstay antimalaria drug, arose in several geographic locations and rapidly spread across continents. This finding upends the long-held notion of some scientists that chloroquine resistance developed independently in only two areas in the mid-20th century and slowly spread to other countries from those sites. The new information implies that resistance to chloroquine and other antimalaria drugs can arise and spread more pervasively than previously thought and argues for careful drug-use monitoring programs.

The new reports appear in back-to-back papers published in the July 18 issue of Nature.

Plasmodium falciparum, the parasite responsible for most deadly cases of malaria, thrives in the tropics and infects about 300 million people annually. One to 2 million people, mostly infants and children, die of the disease each year. The number of cases of malaria worldwide is increasing, mainly because of the evolution of drug-resistant parasites.

Debate regarding the genetic diversity and origin of the parasite has been ongoing since the late 1990s. It was then that a group of evolutionary biologists first proposed a "Malaria Eve" hypothesis to explain the origin of the parasite. By examining 10 genes of the malaria parasite, these scientists proposed that the bug is relatively young -- 3,000 to 5,000 years old -- and genetically similar from place to place, and as such, should not be too difficult to control.

To explore the question in mo
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Contact: Laurie K. Doepel
doepel@nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
17-Jul-2002


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