Researchers have provided new details about the inner workings of a parasitic worm that causes a tropical disease called schistosomiasis, which leads to itchy skin, fever, chills, muscle aches, and liver disease that, in some cases, can be fatal.
The new results, which appear in the September issue of Molecular & Cellular Proteomics, may help design drugs or vaccines against the disease.
Schistosomiasis, a disease affecting up to 200 million people in Asia, Africa, and South America, is spread by parasitic worms called blood flukes that live in fresh water. The worms enter the human body through the skin and move to either the large intestine, small intestine, or the bladder. In the case of a species called Schistosoma mansoni, infection starts when larvae cross the skin and migrate to the large intestine, where they become adults and mate. The females then lay about 300 eggs a day in the blood vessels of the gut wall.
Stuart M. Haslam and colleagues compared the chemicals released by the larvae and eggs to understand how these chemicals help them to infect the human body. They found that although these chemicals are detected by the immune system, the parasite can still spread throughout the body.
In the case of the larvae, the scientists suggest that although the chemicals secreted prompt the human immune system to attack them, these chemicals act as a decoy so that the larvae themselves are not destroyed and can spread at will. The chemicals released by the eggs also attract molecules from the immune system but this time the chemicals fool the immune system into helping them escape from the body through feces and spread in the environment. These results provide new clues as to how the worms infect the human body and may help design drugs that target some of these chemicals in the future.
Article: “Glycomics Analysis of Schistosoma mansoni Egg and Cercarial Secretions,” by Jihye Jang-Lee, Rachel S. Curwen, Peter D. Ashton, Berangere Tissot, William Mathieson, Maria Panico, Anne Dell, R. Alan Wilson, and Stuart M. Haslam
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