Source: National Institutes of Health Director's Blog.
When I volunteered several years ago as a physician in a small hospital in West Africa, one of the most frustrating and frightening diseases I saw was sleeping sickness. Now, an investigator supported by the NIH Common Fund aims to figure out how this disease pathogen manages to evade the human immune system.
Monica Mugnier’s fascination with parasites started in college when she picked up the book Parasite Rex, a riveting, firsthand account of how “sneaky” parasites can be. The next year, while studying abroad in England, Mugnier met a researcher who had studied one of the most devious of parasites—a protozoan, spread by blood-sucking tsetse flies, that causes sleeping sickness in humans and livestock across sub-Saharan Africa.
From her British colleague, Mugnier learned that after a tsetse fly infected with Trypanosoma brucei bites a person, the invading parasitic protozoans cloak themselves in a dense coat of molecules called glycoproteins. When the human immune system detects T. brucei, it marks the protozoans with antibodies that target them for destruction. However, T. brucei possesses the ability to evade such destruction by sweeping off the antibodies and disguising itself in a new set of glycoproteins. This immunological “cat and mouse” game can go on for years. Eventually, the parasite crosses the blood-brain barrier, triggering excessive sleep and life-threatening seizures and coma.
Using a gene-expression approach that she helped to adapt to T. brucei, Mugnier extrapolated that the parasite runs through the 2,000 or so genes that code for its glycoprotein disguises in a matter of months .Read more at directorsblog.nih.gov
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