The Department is well-represented in the results of the 2014 Otago Medical Research Foundation (OMRF) funding round, with 2 of the 7 successful bids. This year there were 38 applications, with the 7 projects investigating aspects of medical research in Otago receiving a total of $144,503.
Congratulations to Dr Robin Simmonds and Dr Heather Brooks, who have been funded for a joint project with Professor Kelly Doran from San Diego State University on the role of a bacteriocin-like inhibitory substance in the pathogenicity of group B streptococci. Dr Jo Kirman will conduct research on Deciphering the memory T cell response to tuberculosis (TB).
Dr Joanna Kirman
Deciphering the memory T cell response to tuberculosis (TB)
JN Lemon Trust, $15,517
The current vaccine against tuberculosis (TB) is ineffective and an improved vaccine is urgently required. In order to develop a new vaccine we must understand the memory immune cells that drive protection against TB. Most new TB vaccines are being designed to stimulate memory CD4 T cell development; however there is no solid evidence to suggest that this is appropriate. We propose to determine whether memory CD4 T cells are required for protection afforded by vaccination by specifically removing these cells after vaccination and before an infectious challenge. This study will aid the development of new TB vaccines.
Dr Robin Simmonds and Dr Heather Brooks and Professor Kelly Doran (Department of Biology - San Diego State University)
Role of a bacteriocin-like inhibitory substance in the pathogenicity of group B streptococci
Southern Victorian Charitable Trust, $22,000
Group B streptococci (GBS) can produce serious invasive disease in humans. Knocking out bliS, a gene encoding a recently discovered GBS endopeptidase, yielded strains of GBS attenuated for persistence in a mouse model. This is the first time an endopeptidase has been shown to play a significant role in the persistence of infection of an animal host by a major human pathogen. This study will establish a biochemical basis for the role played by BliS in the persistence of infection and allow us to establish the potential for therapeutic applications for BliS in the prevention of GBS infections in humans.
