While its common name may make it sound almost whimsical, sleeping sickness, or African trypanosomiasis, is in reality a potentially fatal parasitic infection that has ravaged populations in sub-Saharan Africa for decades, and it continues to infect thousands of people every year.
Researchers at UGA’s Center for Tropical and Emerging Global Diseases have made a discovery that soon may lead to new therapies that cause neither the risks nor the pain associated with traditional treatments for this critically neglected disease.
The CTEGD scientists discovered a specific receptor tucked away in an organelle inside the disease-causing trypanosome parasite that regulates the release of calcium, which is responsible for numerous critical cell functions required for parasite growth and replication.
“This receptor is an attractive drug target,” said Roberto Docampo, the Barbara and Sanford Orkin/Georgia Research Alliance Eminent Scholar and co-author of a paper describing their findings published in the Proceedings of the National Academy of Sciences. “The mechanisms we have identified are critical for the survival of the parasite, so if we can manipulate them, we can stop the infection.”
The calcium receptor identified by the researchers serves as a kind of messenger within the parasite, telling it when to secrete specific chemicals, when to divide and when to spread. They hypothesized that disrupting this system would leave the parasites incapable of growing and replicating within their human and animal hosts.
Docampo and his colleagues tested their hypothesis by watching genetically modified versions of the parasitic cell both in laboratory cultures and in mice. In both cases, the genetically altered parasites with dysfunctional calcium receptors were unable to replicate, and mice in the experimental group remained disease free.
“We knew that these organelles were rich in acidic calcium, but it is not until now that we understand how they released the calcium to control cell functions,” said Docampo, who is a professor of cellular biology in the Franklin College of Arts and Sciences. “Now that we better understand this critical pathway, we may begin thinking about new therapies for sleeping sickness.”