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Antonia Bass

Undergraduate Major: Biotechnology

Future Plans: Biological Sciences Ph.D

Antonia Bass

Antonia Bass was born in Adana, Turkey and grew up in West Palm Beach, Florida. She is pursuing a Bachelor's degree in Biotechnology. Antonia is a member of the National Society of Collegiate Scholars and Pre-Professional Medical Society. Currently, Antonia is the Public Relations Officer for Society for Advancement of Hispanics/Chicanos and Native Americans in Science (SACNAS UCF Chapter). Her current research entails the development of antimicrobial surface coating nanomaterial to be used in bandages. She plans on obtaining her Ph.D. in Biological Sciences and conduct research on infectious diseases.

Mutations in DNA Cytosolic Sensors and Their Effect on Retrovirus Sensing

Conducted at The University of Pennsylvania as a part of the Leadership Alliance Summer Research Program as part of the Summer Research Opportunities Program and McNair Scholars Program.

Mentor: Dr. Spyridon Stavrou, Dr. Susan R. Ross, University of Pennsylvania

Abstract: Retroviruses have evolved to avoid anti-viral host restriction factors that inhibit viral replication. Murine leukemia virus (MLV), a gammaretrovirus, expresses a glycosylated Gag polyprotein (glyco-Gag). We previously showed that glyco-Gag stabilizes the virus capsid and protects the reverse transcription complex (RTC) from several host factors. In contrast, glyco-Gag mutant MLV possesses an unstable capsid that makes the RTC susceptible to recognition by DNA cytosolic sensors, which leads to a type 1 interferon (IFN) anti-viral response. We previously performed an siRNA screen and found two DNA sensors essential for the IFN response, IFI203 and DDX41. In this study, we examined the DNA binding domains (DBDs) of these DNA cytosolic sensors to determine if binding to MLV reverse-transcribed DNA was essential for the IFN response. To do this, we made specific mutations in the DBDs of DDX41 and IFI203 to abrogate DNA binding. Through the use of DNA pull down assays, we will assess the protein-DNA interactions between the cytosolic sensors and the retroviral DNA. We will also test whether these mutated factors are capable of inducing IFN in response to virus. If DNA binding is required, mutation of the DBDs of these cytosolic sensors will dampen the IFN response and allow the retrovirus to replicate more efficiently in the cell. Our results showed that mutations made to the Hinb domain of IFI203 hindered binding to MLVDNA. This study will allow for a better understanding of the interactions between the retroviral DNA and the cellular DNA cytosolic sensors of the cell.