Biologists target lifecycle of deadly parasite

(Press-News.org) 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.

Chagas disease is found across North and South America. Between 6 and 8 million people are believed to be infected, including 300,000 people living in the United States. But many only realize they are infected when they develop symptoms decades later.

“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 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.

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.

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.

END