Brianna has been based at the Burnet Institute since 2018, where she first completed her Bachelor of Science (Honours), with her research project titled ‘the antiviral activity of bat APOBEC3 proteins'. Following the completion of her Honours she worked jointly as a research assistant with the Retroviral Biology and Antivirals Laboratory and the Viral Entry and Vaccines Laboratory.
Brianna commenced her PhD in 2020 at the Burnet through Monash University. She is interested in the prevention of diseases that are endemic in developing nations such as HIV, through combining her areas of interest in microbiology, immunology and international development. Her project is titled ‘the impact of the vaginal environment on epithelial barrier function and HIV susceptibility'. This project aims to determine the impact of the vaginal environment on epithelial barrier function and the implications for HIV susceptibility by investigating the modulation of signalling pathways, gene expression and protein production by estrogen and metabolic products of commensal bacteria in the female reproductive tract.
The vaginal microbiome is a key determinant of a women’s sexual and reproductive health. In contrast to an optimal vaginal microbiome dominated by beneficial lactobacilli which is protective, a non-optimal vaginal microbiome promotes genital inflammation that increases the risk of sexually transmitted infections (STIs) including human immunodeficiency virus (HIV) and preterm birth. Bacterial vaginosis (BV) is the most common clinical manifestation of a non-optimal vaginal microbiome affecting 30% of reproductive age women globally. Current treatment options for BV rely on antibiotics which provide short-term resolution. BV reoccurs in ~60% of women within 6 months. There is an unmet need for effective non-antibiotic-based strategies to target BV and its adverse sequelae.
We aim to determine the role of microbiota metabolites in inactivating HIV and other sexually transmitted infections and their effects on cells of the female reproductive tract.
We investigate how a factor produced by optimal microbiota augments the cervicovaginal mucosal barrier to prevent HIV acquisition.