Leishmania mutant provides insight into disease and may lead to a vaccine

St. Louis, Aug. 28, 2003 -- Researchers at Washington University School of Medicine in St. Louis have shown that Leishmania parasites engineered to lack molecules known as phosphoglycans do not cause disease in genetically susceptible mice. The mutant parasites did, however, survive.

The findings, published in the Aug. 29 issue of the journal Science, may provide an efficient way to study how Leishmania normally persists in the body without triggering symptoms. They also provide new insight into how the parasite causes a disease called leishmaniasis in some individuals and could potentially lead to the development of a vaccine.

"Somehow the persistent Leishmania mutant has found a 'safe' niche within the body that allows the parasite to survive without causing disease and at the same time preventing additional infection," says lead investigator Stephen M. Beverley, Ph.D., the Marvin A. Brennecke Professor and head of the Department of Molecular Microbiology. "This is exactly what happens in normal persistent infections. But we don't know what these persistent parasites look like, what kind of cell they infect or how they interact with the immune system. Our mutant parasite may help answer those questions."

An estimated 12 million people are infected with Leishmania parasites worldwide. Usually the immune system controls the infection and prevents development of leishmaniasis, a disfiguring and sometimes fatal disease. But for some people, such as those with AIDS who have a suppressed immune system, the parasites become active and trigger leishmaniasis. In fact, the disease is a common complication of AIDS in endemic regions including the Mediterranean basin and Southern Europe.

Persistent parasite infections are usually difficult to study, according to Beverley, because it can take six months to a year to establish the persistent infection before research can begin. Postdoctoral researcher and first author Gerald Spth, Ph.D, avoid

Contact: Gila Z. Reckess
Washington University School of Medicine

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