Targeting the Lifecycle of a Deadly Parasite
Chagas disease kills thousands each year.
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Chagas disease is often called a silent killer because many people don’t realize they have it until complications from the infection kill them.
Researchers at the University of Cincinnati are exploring ways to interrupt the lifecycle of the parasite behind the illness, offering hope of developing a cure.
The disease is spread by parasites found in kissing bugs, which suck the blood of people when they are sleeping. The bugs typically bite victims around their faces, which gives them their ironically sweet-sounding name. The bugs transmit the internal parasites in their poop, which infects the bloodstream of human hosts through the bite wounds.
The study was published in the journal mBio, from the American Society for Microbiology.
Chagas disease is found across North and South America. Between 6 and 8 million people are believed to be infected, including 300,000 living in the United States, according to federal health data. But many only realize they are infected when they develop symptoms decades later. The parasites cause gastrointestinal and neurological impairments and enlargement of the heart, which can lead to cardiac arrest.
“The main issue with Chagas disease as a public health problem is that most people don’t know they’re infected until symptoms appear and it’s too late to treat them,” UC Assistant Professor Noelia Lander said.
In her molecular parasitology lab, Lander and her students are studying the complex lifecycle of the parasite to find vulnerabilities to exploit.
The parasite is a tiny single-celled organism that undergoes four lifecycle changes to survive and reproduce on its odyssey from the digestive system of an insect to the bloodstream of a human and back. Along the way, it must be able to withstand dramatic differences in its environment such as acidity, temperature and the availability of nutrients.
The parasite attaches itself to the hindgut of the kissing bug’s digestive tract with a tail called a flagellum and transforms to be infective. And when poop from the kissing bug infects a bite wound, the parasite enters a person’s body where it infects cells of all kinds: nerve cells, muscle cells, white blood cells. Inside these cells, it transforms again, losing its flagellum and replicating many times. Eventually, the cell bursts, releasing infective forms that can spread the infection to other cells.
The parasite has been living on Earth for millions of years — long before people.
“I know the parasite is the enemy. But I’m impressed by the mechanisms the parasite has to survive during its lifecycle,” Lander said. “The goal is to find its weaknesses to fight the disease.”
UC graduate Joshua Carlson was lead author of the paper. Co-author and UC doctoral student Milad Ahmed said the parasite hides within the cells it infects in human tissues, helping it to evade both the immune system and medications. Once the disease becomes chronic, treatments become significantly less effective, he said.
“The significant genetic diversity of the parasite further complicates efforts to develop effective vaccines or universally applicable treatments,” Ahmed said.
Researchers used gene-editing tools to manipulate the genes of the parasite. The aim was to identify the location and function of one of the proteins that helps the tiny parasite adapt, study co-author and UC Assistant Professor Miguel Chiurillo said.
Chiurillo said UC researchers targeted a signaling pathway that controls cues for the parasite’s survival within the kissing bug.
“Two main functions are important to survive inside a kissing bug: to replicate inside the bug and to attach to the digestive tract,” he said. “If we can block this interaction, we can stop the spread of the disease.”
Lander said interrupting the parasite’s lifecycle is a promising target for future medical treatments.
“If the parasite can’t transform during its lifecycle, it won’t survive,” she said.
The research was supported by the National Institute of Allergy and Infectious Diseases.
Reference: Carlson J, Ahmed M, Hunter R, et al. TcCARP3 modulates compartmentalized cAMP signals involved in osmoregulation, infection of mammalian cells, and colonization of the triatomine vector in the human pathogen Trypanosoma cruzi. mBio. 2025;0(0):e00994-25. doi: 10.1128/mbio.00994-25
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