About Professor Nicholas Hunt
Ever since I was at primary school I have been fascinated by the intricacy of biological systems, in particular the human body. The way in which the myriad processes that support our normal body functions are coordinated is awe-inspiring. To have a career spent unravelling this and the problems that occur in diseases like malaria and meningitis is a privilege.
Nick Hunt is well-known for his studies of the severe illness caused by malaria infection and his interest in free radical biology and inflammation.
Nick Hunt is Professor of Pathology (since 1989). His research interests are in the immunopathology of infectious diseases, particularly malaria and meningitis. His laboratory is also active in studying a very important biochemical pathway, the kynurenine pathway of tryptophan metabolism, which has a variety of physiological and immunological roles as well as being implicated in several diseases. In 2005 Dr Helen Ball in the lab discovered a new enzyme that regulates this pathway. Since 1989 Nick has supervised 20 PhD students to completion and two more have recently submitted their theses. Almost all past students are in academic research positions at institutions including Harvard, University of Oxford, John Curtin School of Medical Research, or are in positions in the Australian biotechnology industry. He has examined 26 PhD theses since 1989. Since 1989 Nick has spoken by invitation at 38 International and 27 National scientific conferences, including several Plenary or Keynote presentations.
Scientific highlights in malaria research since 1995 include:
- Demonstration of glial involvement in experimental cerebral malaria (CM), since confirmed by others in the human disease; these well-cited observations added a new dimension to consideration of immune system involvement in CM. Increased permeability of the blood-brain barrier to proteins was shown in murine CM, explaining how cytokines and malaria antigens can enter the brain and activate glia.
- Showing that the kynurenine pathway of tryptophan metabolism is activated in the brain in murine CM, then confirming this in human severe malaria; this gave a possible explanation for some symptoms of CM, and indicated a potential therapeutic route.
- Demonstrating that the mouse model of CM can be used to investigate the mechanisms of brain metabolic changes in CM. Current findings suggest that cytokines may drive the changes in brain bioenergetics that are observed as increased brain lactate and alanine in human and murine CM.