BiographyPeter White is a Professor at the University of New South Wales in Australia. He is a molecular virologist with a particular interest in antiviral development, viral evolution, paleovirology and pandemic noroviruses. He has a breadth of experience in the development of novel molecular assay systems to investigate viral infections. His group also has interests in hepatitis viruses and antibiotic resistance.
Following a BSc (Hons) in Biotechnology from King’s College London (1992), Peter completed a PhD at University College, London (1996) in molecular microbiology. Prof White commenced his Postdoctoral research studies at Macquarie University, Sydney, as a recipient of a Royal Society Fellowship and later worked as Hepatitis Group Leader at the Prince of Wales Hospital until joining the University of New South Wales in 2003. He is also an enthusiastic teacher, having convened the third year science course Viruses and Disease for 13 years at UNSW.
Areas of Research / Professional Expertise
Infection with hepatitis C virus (HCV) contributes one of the most important health care burdens both in Australia and worldwide with more than 170 million people infected. The majority of infected individuals develop persistent infection (70%) and an associated risk of progressive fibrosis, cirrhosis, liver failure and hepatocellular carcinoma.
In the field of HCV, Peter has contributed several landmark publications in relation to replication, molecular tools, HCV epidemiology, reinfection and antiviral agents. Using modern molecular biology techniques, next generation sequencing and bioinformatics, the group studies the replication and evolution of HCV within chronically infected individuals. HCV has a positive sense RNA genomes that replicates in the cytoplasm of the infected cell via minus-strand RNA intermediates. The lack of proof reading activity of the polymerase means that these viruses exist in an individual as a population of closely related variants. Varied or complex viral populations are thought to be important in evasion of the host immune response. The viral polymerase is also a key player in the evolution of the virus and the group makes recombinant polymerases, using bacterial expression systems from a range of HCV genotypes for enzymatic and evolutionary studies.
Norovirus (NoV) is the leading cause of outbreaks of viral gastroenteritis worldwide and is associated with over 200,000 deaths per year in the frail, immunodeficient and malnourished populations in developing countries. Each year norovirus cause 64,000 episodes of diarrhoea requiring hospitalisation and 900,000 clinic visits among children in industrialized countries. NoV transmission occurs primarily from person-to-person, however, transmission through contaminated food and water makes this virus the most significant viral pathogen in food and water outbreaks of gastroenteritis. Pandemics of acute gastroenteritis are associated with a genetic lineage of Noroviruses called GII.4. Peter's research over the last five years has examined evolutionary processes that have led to the emergence of pandemic noroviruses.
Progress made so far in the molecular biology of norovirus by White’s group has revealed the presence of a particularly important genotype of the virus, known as Norovirus Genogroup II, genotype 4 (GII.4) (over 30 other genotypes of Norovirus exist), as the cause of global pandemics of gastroenteritis, accounting for more than 80% of all Norovirus infections. Since the first global pandemic of acute gastroenteritis in the mid 1990s, Peter White's group has been instrumental in identifying and tracing the cause - pandemic GII.4 Noroviruses. Seminal work by White’s group has shown that the emergence of pandemic GII.4 Noroviruses is driven by two factors; i) the generation of point mutations in antigenic regions of the viral capsid, in an analogous manner to influenza, and ii) through recombination between two Noroviruses during a co-infection. Current research from the group on both human and mouse norovirus involves development of antiviral agents and research into the host innate immune response, molecular epidemiology, pathogenesis and replication.
Peter's group has a strong collaboration with the New South Wales Department of Health, which monitors outbreaks of gastroenteritis for the State. Peter established the Australian and New Zealand Norovirus Surveillance Network, a network of large testing laboratories in major cities around Australia and New Zealand. The Network collectively monitors the emergence of new epidemic and pandemic viruses linked to outbreaks of Norovirus associated gastroenteritis. This network directly links in with two other networks, the Food-borne Viruses in Europe (FBVE) network (13 EU countries) and CaliciNet run by the Centres for Disease Control (USA and Canada), to form the global Norovirus surveillance network, termed NoroNet. Collaborative work by the group was published in the Journal of Infectious Disease in 2009.
Development of small compound viral non-nucleoside viral polymerase inhibitors HCV and norovirus both have positive sense RNA genomes that replicates in the cytoplasm of the infected cell via minus-strand RNA intermediates. The lack of proof reading activity of the polymerase means that these viruses exist in an individual as a population of closely related variants. Varied or complex viral populations are thought to be important in evasion of the host immune response. Using our established methodology we have produced highly purified, soluble and active recombinant RdRps from a range of HCV and norovirus genotypes and strains, using Escherichia coli expression systems.
In the field of virology, there is an extremely active hunt for antiviral agents to treat and prevent viral infections. Current therapies for HCV only work in around 50-80% of infected patients and have adverse side-effects, and no antivirals have so far been developed for norovirus infections. One target for drug development is the viral RNA dependent RNA polymerase (RdRp) because of its key role in replication. High throughput screening (HTS) is a standard platform used to identify lead chemical compounds for drug development. The aim of the antiviral program is to conduct high throughput screening (HTS) campaigns against the HCV and norovirus RNA polymerases to identify and characterise lead compounds and derivatives for potential antiviral therapy.