Yekateryna Sinitsyna
Pronouns: She/her
Research Mentor(s): Michal Olszewski
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine, Pulmonary and Critical Care Medicine / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 4 – 2:40pm – 3:30 pm
Room: League Ballroom
Authors: Yekateryna Sinitsyna, Michal Olszewski, Kristie Goughenour
Presenter: 72
Abstract
The pathogenicity of microbes is a determined group of features defined as virulence factors, which in turn are coded by pathogen virulence genes. Cryptococcus neoformans is a fungus predominantly infecting people with a weak immune system but its ability to invade the hosts is also coded by a large group of virulence genes. The flavin carrier protein 1 (Flc1) has been shown in other fungi to help regulate stress response. However, it’s role in C. neoformans virulence is unknown. To test this, we performed an intra-tracheal infection of C57BL/6J mice using an flc1 gene knockout strain of C. neoformans (flc1?). Mice survive mutant infection indicating flc1 is required for virulence. The Wildtype and the flc1? + FLC1 infected mice were observed to have started to die 10 days post infection while the flc1? infected mice were able to survive the full 21-day study. Observing the fungal burdens of C. neoformans in the lungs showed the difference between Wild Type (H99), flc1? mutant and Flc1 complement with the flc1? mutant having a 2 log decrease compared to the Wild Type or complement in CFUs (colony forming units) on day 3 post-infection. As we saw a drop in C. neoformans by 3 days post infection, the reduction in virulence must be due to innate immunity clearance as this is too early for adaptive immunity to kick in or a deficiency in fitness. But there is a reduction in fitness because the mice are still dying from the fungal burdens even after clearing the fungi. In the end, it is required for C. neoformans virulence.
Biomedical Sciences, Interdisciplinary, Natural/Life Sciences
