Evan Alexander Scott
University of Virginia, VA·Biomedical Engineering
Chagas disease is caused by Trypanosoma cruzi, a single-celled parasite spread in the Americas, and it remains a serious public health problem in need of new treatments. The parasite can infect nearly any cell with a nucleus and persists in tissue reservoirs, especially fat tissue, creating a long-term risk that the infection flares up again.
- Fields
Biomedical Engineering
Microbiology & Immunology
Pharmacology
- Topics
Chagas disease
American trypanosomiasis
Trypanosoma cruzi
- Grants
- 1 known grant, through May 2029
What they work on
- Validate a combination nanotherapy that both dampens local immune attack on the heart and kills parasites, testing whether it treats established chronic Chagas cardiomyopathy without reactivating Trypanosoma cruzi.
- Determine the efficacy of the combination nanotherapy across multiple T. cruzi strains, including clinically relevant strains from an endemic region in Brazil.
- Engineer nanocarriers that home to parasite reservoirs in adipose tissue, the main hiding place for most T. cruzi strains, to eliminate infection at specific reservoir sites.
- Optimize nanocarriers loaded with a new thiophene-based antiparasitic compound and test them against benznidazole-resistant T. cruzi strains and patient-derived clinical isolates.
More about the research
About one third of infected people develop chronic Chagas cardiomyopathy, a lasting heart disease that is the world's leading cause of infection-driven heart muscle inflammation. Treating it is hard: calming the inflammation in the heart can weaken the immune defenses that keep the parasite in check, which risks waking up hidden reservoirs. The two long-standing drugs, benznidazole and nifurtimox, are often toxic and do not work well against the heart disease.
Why it matters
Chronic Chagas cardiomyopathy affects roughly a third of people infected with Trypanosoma cruzi and is the leading cause of infectious heart muscle inflammation worldwide, yet current drugs are toxic and largely ineffective against it. Nanotherapies that suppress heart inflammation locally while still clearing the parasite, together with a less toxic alternative drug for resistant strains, could offer patients treatment options that today do not exist.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Arthur Gunzl
University of Connecticut, CT·Microbiology & Immunology
Determine how the cyclin-dependent kinase CRK9 controls spliced leader trans splicing in Trypanosoma brucei, including whether it phosphorylates the splicing factor TSR1, using parasites with chemically inhibitable analog-sensitive CRK9.
Christian Tschudi
Yale University, CT·Microbiology & Immunology
Determine how T. brucei parasites receive the signal to begin making the metacyclic VSG (mVSG) coat that lets them infect mammals, using parasites induced to develop by switching on the RNA-binding protein RBP6.
Juergen Bosch
Case Western Reserve University, OH·Biochemistry
Improve existing anti-malarial antibodies and design new ones based on humAb826827 and 864865, which bind PvAMA1, a Plasmodium vivax surface protein required to invade cells, by computationally generating about 1,000 antibody scaffolds per target epitope.
The school
University of Virginia: 43 labs on PI Pages, $814M a year on research, 413 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.