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Aylla von Ermland, a Ph.D. student in the ’s Department of Cellular Biology, recently received a pre-doctoral fellowship from the American Heart Association to fund two years of her research.

Growing up in Brazil, von Ermland learned about Chagas disease at an early age. Carlos Chagas was a Brazilian physician who is credited with discovering the disease in 1909. Chagas disease is an endemic parasitic infection caused by Trypanosoma cruzi. Chronic infection often leads to fatal heart failure. It is estimated that up to 4.6 million Brazilians are infected with T. cruzi and 25.4 million are at risk of contracting the disease.

Human Chagas disease, which causes damage to the heart, is most prevalent in Central and South America. Although cases of human Chagas disease are rare in the United States, working dogs and wildlife are at risk as both the parasite and the insect that transmits it are present throughout the U.S. There are currently no vaccines; furthermore, current treatments often have serious side effects and are not always effective in curing the disease.

“Being from Brazil, we hear about Chagas from a young age,” said von Ermland. “From early on I was interested in science and in my first year as an undergraduate at the University of São Paulo I had the opportunity to do parasitology research.”

While still an undergraduate, von Ermland participated in a study abroad program where she spent a semester in the laboratory of Rick Tarleton, cellular biology professor and member of the .

“My experience as an exchange student is what brought me back to UGA and the Tarleton �����Դ�ɼ��� Group for graduate school,” said von Ermland. Now as a graduate student in Tarleton’s laboratory, she is continuing her research on T. cruzi.

The parasite is good at evading the human immune response through multiple mechanisms. The parasite expresses a variety of highly diverse surface proteins, and this might be a key reason they can slip past our defenses.

“Studies have shown extensive genetic differences in surface proteins among different isolates of T. cruzi,” said von Ermland. “But we don’t know how long it took for these variations to occur – there are a lot of unanswered questions.”

Von Ermland hopes to answer some of these questions with her AHA fellowship. She will study the scale and pace of recombination among multigene families that encode surface proteins during short- (~3 months) and long-term (~1 year) infection in mice.

“Preliminary results show accumulation of recombination among multigene families,” said von Ermland. “But it is uncertain what the implications of this genetic variability are in the ’real world’.”

To get a clearer picture of multigene family recombination in recent isolates of the parasite, another part of her research focuses on uncovering the genetic variation in parasite samples collected from naturally infected dogs and non-human primates in the U.S. and humans in South America.

“The ability of T. cruzi to alter the many proteins on its surface makes it a “moving target” for the immune system,” said Tarleton. “Understanding how dynamic and rapid this process is could help efforts to enhance immune recognition and control of the infection.”