Burnet Institute studies ranging from innovative antiviral strategies, to the development of new diagnostics, and research focused on vaccine development have attracted valuable funding from the Australian Centre for HIV and Hepatitis Virology Research (ACH2).
“A terrific outcome” was how Burnet Head of Life Sciences, Professor Gilda Tachedjian described the grants awarded to Professor Heidi Drummer, Associate Professor David Anderson, Dr Rob Center, Dr Jess Howell, Dr Andy Poumbourios, Dr Bruce Wines and Dr Jack Richards. Professor Tachedjian also received a grant.
“Congratulations to our Life Science Discipline researchers and their co-CIs for winning ACH2 funding for translational research in HIV and hepatitis virology,” Professor Tachedjian said.
“The focus of the successful research grants is centred on vaccines, prevention and immunotherapy; diagnostics and prognostics; and antiviral strategies.
“It shows the excellence of our work and the translational nature of our work in taking fundamental research and going that next step to develop a vaccine, diagnostic or antiviral microbicide.
“We’re thrilled to have support from ACH2 to be able to do this important work.”
The funded work focuses on:
- Professor Gilda Tachedjian: Optimisation of a gel for enhancing the vaginal environment and microbiome (EVE-M) to prevent HIV transmission
- Professor Heidi Drummer: Low cost method of manufacture for hepatitis C vaccine
- Associate Professor David Anderson: Development of quantitative HBV detection at point-of-care: proof of concept
- Associate Professor Jack Richards: Development of a point-of-care test for hepatitis B DNA
- Dr Jess Howell: Utility of a rapid point-of-care ALT1 test to monitor disease progression and treatment eligibility in people living with hepatitis B
- Dr Andy Poumbourios: Immunogenicity of novel polyvalent HIV glycoprotein vaccines
- Dr Rob Center: Immuno-silencing the HCV E2 glycoprotein non-neutralizing face
- Dr Bruce Wines: Harnessing the glycan reactivity of PGT121‐like bNAbs for potent FcγRIII mediated killing of Env expressing target cells.