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Genetic Research Offers Insights Into Form of Malaria

P. vivax causes 300 million cases of the disease each year


WEDNESDAY, Oct. 8 (HealthDay News) -- The genetic structure of the malaria-causing Plasmodium vivax parasite has been described by an international team of researchers, who said the information could help in the fight against malaria.

The majority of research into malaria has focused on the Plasmodium falciparum parasite, which causes the most virulent form of the disease. But P. vivax and other parasites of the same genus as P. falciparum also cause malaria.

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It's believed that P. vivax causes nearly 300 million cases of malaria worldwide each year. While it is rarely fatal, P. vivax can cause severe malaria and resistance to some drugs, the researchers said.

The U.S. Institute for Genomic Research-led study found that P. vivax is far more similar to P. falciparum than expected. The researchers identified only 150 genes specific to P. vivax.

The study also found that P. vivax may have unique routes of invasion for penetrating blood cells in which the parasite resides and multiples during its life cycle. These alternative routes of infection haven't been noted in previous research and the genetic information necessary for this to happen is written in the genome of P. vivax, the researchers said.

The findings are published in the Oct. 9 issue of Nature.

Even though P. vivax causes 300 million cases of malaria each year in countries such as Brazil, India and Papua New Guinea, there has been a tendency to underestimate the importance of research into this form of malaria, the study authors noted.

They said research into P. vivax should be included in the funding schedules of the nations leading the global fight against malaria.

More information

The U.S. Centers for Disease Control and Prevention has more about malaria.



-- Robert Preidt

Copyright © 2008 ScoutNews, LLC. All rights reserved.
Last updated 10/8/2008

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SOURCE: Institut d'Investigacions Biomediques August Pi i Sunyer, news release, Oct. 8, 2008


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