The study found that parasites engineered to lack the molecule known as lipophosphoglycan (LPG) were ten times more vulnerable to attack by an immune defense known as complement, which is found in the bloodstream. And although parasites that lack LPG easily enter macrophages (immune cells that the parasite normally infects), they were quickly destroyed once inside the cells.
The findings are published online and in the Aug. 5 issue of the Proceedings of the National Academy of Sciences.
"This study helps us better understand how these parasites are transmitted and how they establish infections," says principal investigator Stephen M. Beverley, Ph.D., the Marvin A. Brennecke Professor of Molecular Microbiology and head of the department. "It also could help efforts leading to the development of a vaccine to prevent this devastating disease."
About 12 million people are thought to be infected with leishmania parasites worldwide. The parasite is spread by the bite of infected sand flies and can cause leishmaniasis, a sometimes fatal and disfiguring disease.
Cutaneous leishmaniasis causes open, slow-healing and sometimes disfiguring skin sores. Visceral leishmaniasis spreads to several organs and is usually fatal if left untreated. About 1.5 million new cases of cutaneous leishmaniasis and 500,000 new cases of visceral leishmaniasis occur each year. The mainly tropical and subtropical disease takes its greatest toll in poor countries such as India and war-torn countries such as Sudan. It also arises as an opportunistic infection in people with AIDS.
Beverley and a group of his colleagues genetically engineered a strain of leishmania parasites that lacked LPG. They tested the ability of these modified parasites to cause infec
Contact: Darrell E. Ward
Washington University School of Medicine