Immunology and Cell Biology            

Cell-Cell Interaction Group | Viral Engineering and Cytokine Group - Immune Regulation and Vaccine Development Laboratory - Synthetic Vaccines Laboratory | Immunity and Immunopathology in Infectious Disease | Viral Immunology Group - Immunology Laboratory | Experimental Haematology Laboratory | Staff

Introduction

The Division of Immunology and Cell Biology is comprised of a number of research groups that investigate fundamental aspects of cell biology, with a major interest being the immune system.
Research undertaken by the Division includes investigations of viral replication, analyses of the immune response to viral infections, development of HIV and cancer vaccines, studies of the processes involved in programmed cell differentiation and death, and research on the processes of inflammation, haemapoiesis, tumour angiogenesis and tumour metastasis. Tugofwar. Photo:Rohan Baker
Professor Parish leads his team at the School Christmas party.

The pursuit of long term basic science goals make up most of the Division's work but this is balanced by attempts to translate fundamental discoveries into clinical applications. The latter include the possible application of anionic sugar molecules as novel anti-inflammatory or anti-cancer drugs and naked DNA and recombinant poxviruses as vaccines for prevention of certain infectious diseases or treatment of cancer. More detail of these various themes is given in each Group or Laboratory report.


Chris Parish
Division Head

 

Essays

Cell-Cell Interaction Group
Professor Chris Parish

The Cell-Cell Interaction (CCI) group has been working for a number of years on the molecular basis of cell adhesion, cell migration and cell invasion, with a particular emphasis on the immune system, tumour metastasis and the growth of new blood vessels (angiogenesis). Of particular interest has been the role of anionic carbohydrates, such as heparan sulfate, in these processes. In addition the Group aims to apply its basic research findings to the development of new drugs which inhibit inflammation, cancer spread and angiogenesis. Considerable amounts of external research funds have been obtained to finance the drug discovery programs. Recent research highlights are:-

  • Following the recent cloning of the enzyme heparanase, a key enzyme involved in degradation of the extracellular matrix by invading tumour cells and by leukocytes entering inflammatory sites, the CCI group has gained considerable information about the active site of the enzyme. This information will be invaluable for the design of more effective heparanase inhibitors.

  • The group has had considerable experience in designing sulfated oligosaccharide-based compounds as drug candidates, this part of the group's research being supported by a large R and D grant from Progen Industries, Brisbane. Sulfated oligosaccharide-based inhibitors of the heparanase enzyme have been synthesised and identified, with a sulfated oligosaccharide, termed PI-88, being found to be a potent inhibitor of angiogenesis and heparanase activity. Preclinical testing has shown that PI-88 can inhibit primary tumour growth and tumour metastasis. By the end of 2000 the drug had successfully completed phase I clinical trials in healthy volunteers and cancer patients, with phase II trials in cancer patients planned for 2001.

  • A very productive collaboration has developed recently with Professor Martin Banwell, Research School of Chemistry, ANU in which sulfated pseudo-sugars are being synthesized as heparan sulfate mimetics. This project is also being funded by our commercial partner, Progen Industries. Although the initial aim of this collaboration is to produce better heparanase inhibitors, sulfated pseudo-sugars are also being examined as potential anti-angiogenics, anticoagulants, antiviral agents and antilipaemic drugs.

  • The group has been studying the plasma protein, histidine-rich glycoprotein (HRG), for many years, particularly regarding the ability of the protein to inhibit cell adhesion by masking cell surface carbohydrates. Recently, however, it became clear that HRG plays an important role in the immune system by preventing the insolubilisation of complexes between antibody and antigen (termed immune complexes). In fact HRG also assists in the uptake of these complexes by phagocytic cells. Thus HRG is probably a key molecule in aiding the elimination of immune complexes from the circulation. In fact, deficiencies in HRG may lead to immune complex-associated diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosis (SLE). This is an extremely novel area of research which is being pioneered by the CCI Group.

  • A productive collaboration has developed with Dr Joe Altin, BaMBi, ANU in which a procedure has been devised to tether the extracellular domains of cell surface receptors to cell membranes. This technology has been used to graft costimulator molecules, such as CD40 and CD80, onto tumour cell surfaces to produce better cancer vaccines. The technology is also being used to target liposomes containing cytotoxic drugs to sites of angiogenesis in humans, such an approach being potentially a potent means of inducing tumour regression.


Viral Engineering and Cytokine Group
Professor Ian Ramshaw

There is an urgent need for an HIV/AIDS vaccine for developing countries. More than 16 million people have died of AIDS, more than 34 million people are living with HIV and nearly all will die of AIDS within the next two decades. Although other measures have slowed the spread of AIDS only an AIDS vaccine can end the HIV/AIDS pandemic. This year the US National Institutes of Health awarded a A$30 million contract to a consortium of Australian researchers to develop and trial an HIV/AIDS vaccine. This is the largest grant yet given to an Australian research team from an international agency. The members of the consortium include the John Curtin School of Medical Research, the University of Melbourne, the University of New South Wales, the University of Newcastle and the CSIRO. The HIV/AIDS vaccine approach involves both prime boost immunisation with DNA and recombinant fowlpoxvirus vectors with the co expression of immune-enhancing cytokine genes. It is gratifying that both technologies used in this novel vaccine approach were developed from fundamental research carried out at the JCSMR over the last decade. Although these vaccine strategies lead to unprecedented levels of immunity there is still a need to develop new approaches to cover the genetic diversity seen with HIV, this area will be a major focus of our future research.

Immune regulation and vaccine development laboratory
Professor Ian Ramshaw

The focus of our research is to study the factors important in generating high levels of protective immunity to vaccination. In particular, we are concentrating on the use of prime boost immunisation to stimulate high levels of cell-mediated immunity. We have been studying why this vaccination strategy generates such a powerful response. Using a tetramer staining technique we have been able to show that DNA vaccines are able to induce very effective or high avidity T cells which are then expanded by boosting with a recombinant fowlpoxvirus vaccine encoding the same vaccine antigen. The quality of an immune response generated by a particular vaccine strategy may therefore be as important as the levels of immunity induced. Vaccines, that generate T cell populations of high avidity, optimising the early detection of infected cells, offer new hope for development of effective prophylaxis against pathogens such as HIV, which have presented major problems for vaccine development.

Synthetic Vaccines Laboratory
Dr Scott Thomson

Research in the laboratory focuses on developing new vaccine and therapeutic strategies for a broad range of human diseases including viral infections, autoimmunity and cancer. The laboratory is also closely involved with the Australian HIV Vaccine Consortium, which this year was awarded the largest medical research grant in Australia to carryout clinical trials in Australia and SE Asia. The HIV consortium work carried out this year in the lab has involved beginning modification of HIV sequences from two HIV-1 strains and constructing two DNA vaccines, which will be used as the first component of the immunisations in the clinical trials.

The laboratory has recently developed a new vaccine strategy. This technology will allow the development of more effective and safe vaccines using a synthetic super-attenuation approach. It can also be used to combine multiple cancer antigens safely into a single vaccine.

Older technology based on polyepitope vaccines, where multiple contiguous T cell epitopes are used to design synthetic antigens, is continuing to be developed through collaborations with the CRC for vaccine technology (Queensland Institute of Medical Research) and the Sir Albert Sakzewski Virus Research Center. These collaborations are developing vaccines against Epstein-Barr virus the cause of glandular fever and Human Papilloma virus which is leading cause of cervical cancer respectively.

The laboratory given its interest in developing novel vaccines has also been researching various immunomodulatory molecules which when combined with our various antigen technologies could be applied to diseases such as autoimmmunity, allergy and cancers

 

Immunity and Immunopathology in Infectious Disease
Dr Eva Lee, Dr Mario Lobigs and Dr Arno Müllbacher

The general aims of the program are first, to generate new knowledge relevant to our understanding of the fundamental properties of immune responses at the molecular, cellular and whole system level with particular emphasis on immune responses against viruses and second, to study virus/host interactions at the cellular and molecular level and through this devise strategies for the prevention of viral disease.

The members of the program have wide expertise in immunology, immunopathology and molecular virology. Our current investigations focus on the different functions of cytolytic effector molecules, MHC class I antigen presentation, T lymphocyte responses against infection with viruses, bacteria and fungi, the cytotoxic T memory response, virus/host interactions in flavivirus assembly and replication, viral immune evasion strategies, and apoptotic cell death, including death induced by T cells. A large number of virus models including flaviviruses, poxviruses, influenza and parainfluenza viruses, alphaviruses, herpes viruses and adenoviruses are employed in these studies. The availability and establishment by our laboratories of gene targeted mice defective in immune effector molecules including perforin, the granzymes, and Fas receptor/ligand has allowed us to elucidate important host/parasite relationships in the context of the host immune response. Another important approach which is currently applied widely in the group is that of reverse genetics using full-length cDNA copies of flavivirus RNA genomes. These allow the in vitro synthesis of infectious viral RNA and thus structure/function studies in flavivirus replication and pathogenesis.

Progress in our research in the last year is summarized below.

Proteolytic processing of peptides in the lumen of the endoplasmic reticulum for antigen presentation by major histocompatibility Class I
We have tested the hypothesis that MHC class I molecules are actively involved as protease in the production of natural MHC class I ligands. First, the structure of a class I molecule was analyzed for homology with catalytic sites of known proteases. While several clusters of amino acids in the restriction element resembled protease active sites, structural discrepancies and the influence of nearby residues suggest that these sites are unlikely to have protease activity. Second, we have tested the presentation of viral cytotoxic T cell determinants with affinity for the same restriction element (H-2Kd or Kk), when targeted as tandem peptides into the endoplasmic reticulum. Peptide transporter-defective cells were used to exclude cleavage of the tandem peptides by cytosolic proteases. Cleavage by signal peptidase of the tandem peptides was ascertained. The C-terminal peptides in the tandem arrays were almost exclusively presented, suggesting that an aminopeptidase in the endoplasmic reticulum degraded the N-terminally positioned peptides. This result is inconsistent with a MHC class I-catalysed cleavage following binding of longer peptides in the cleft of the restriction elements. Finally, we conclusively show that an aminopeptidase in the endoplasmic reticulum is also involved in antigen presentation in cells with a functional peptide transporter.

Substitutions at the putative receptor-binding site of an encephalitic flavivirus alter virulence and host cell tropism and reveal a role of glycosaminoglycans in entry
The flavivirus receptor-binding domain has been putatively assigned to a hydrophilic region (FG loop) in the envelope (E) protein. In some flaviviruses this domain harbors the integrin-binding motif, Arg-Gly-Asp (RGD). One of us has shown earlier that host cell adaptation of Murray Valley encephalitis virus (MVE) can result in the selection of attenuated variants altered at E protein residue Asp390, which is part of an RGD-motif. Here, a full-length, infectious cDNA clone of MVE was constructed and employed to systematically investigate the impact of single amino acid changes at Asp390 on cell tropism, virus entry, and virulence. Each of ten different E protein 390 mutants was viable. Three mutants (Gly390, Ala390, and His390) showed pronounced differences from an infectious clone-derived control virus in growth in mammalian and mosquito cells. The altered cell tropism correlated with (1) a difference in entry kinetics, (2) an increased dependence on glycosaminoglycans (determined by inhibition of virus infectivity by heparin) for attachment of the three mutants to different mammalian cells, and (3) the loss of virulence in mice. These results confirm a functional role of the FG loop in the flavivirus E protein in virus entry and suggest that encephalitic flaviviruses can enter cells via attachment to glycosaminoglycans. However, it appears that additional cell surface molecules are also used as receptors by natural isolates of MVE and that the increased dependence on glycosaminoglycans for entry results in the loss of neuroinvasiveness.

Stimulation of Dengue Virus Replication in Cultured Aedes albopictus (C6/36) Mosquito Cells by the Antifungal Imidazoles Ketoconazole and Miconazole
Replication of dengue type 3 virus in Aedes albopictus C6/36 cells was enhanced more than 50-fold by addition of the anti-fungal imidazole derivative ketoconazole within the first four hours of infection. The stimulatory effect was reflected in the yield of infectious virus and in levels of viral RNA and protein synthesis. Enhanced yields were observed also for other flaviviruses, including dengue type 2 virus and Murray Valley encephalitis virus. Increased yields of dengue type 3 virus were not observed in African green monkey kidney (Vero) cells, human monocytic (U-937) cells, nor the mosquito Toxorhynchites amboinensis (TRA-171) cells.

Mechanisms of cell killing by cytotoxic T cells
Cytotoxic T (Tc) cells deficient in perforin lyse Fas-negative targets after lengthy incubation periods. This process is independent of granzymes and killing occurs via the Fas pathway for the following reasons: Interaction of perforin deficient Tc cells with Fas-negative targets leads to an upregulation of Fas which is dependent on antigen recognition, de novo synthesis and transport of proteins to the target cell surface. Treatment of effectors with Brefeldin A but not with the exocytosis inhibitor concanamycin inhibited this process. Lysis of targets is inhibited by anti-Fas antibodies, soluble mouse Fas-Fc and the caspase-cascade inhibitor, crm-A. Targets from Fas Ð mutant lpr mice are refractory to lysis and Tc cells from mice deficient in Fas- and perforin-mediated lysis, do not lyse Fas-negative targets. The possible relevance of this exocytosis-independent cytolytic process may be found in the regulation of T cell activity and control of pathogens.

Role of granzymes in recovery from viral infections
Analysis of perforin-deficient mice has identified the cytolytic pathway and perforin as the pre-eminent effector molecule in T cell-mediated control of virus infections. We have now shown that mice lacking both granzyme A (gzmA) and granzyme B (gzmB), which are, beside perforin, key constituents of cytolytic vesicles, are as incapable as are perforin-deficient mice to control primary infections by the natural mouse pathogen ectromelia, a poxvirus. Death of gzmAxgzmB double KO mice occurred in a dose-dependent manner, in spite of the expression of functionally active perforin and the absence of an intrinsic defect to generate splenic cytolytic T cells. This establishes that both gzm A and gzmB are indispensable effector molecules acting in synergy with perforin in granule exocytosis-mediated host defence against natural viral pathogens.

Cytotoxic T cell response to Flaviviruses
We have investigated the reactivities of cytotoxic T (Tc) cells against the two immunodominant, H-2Kk-restricted determinants from the flavivirus Murray Valley encephalitis virus (MVE), MVE1785 (REHSGNEI) and MVE1971 (DEGEGRVI). The respective Tc cell populations cross-reactively lysed target cells pulsed with determinants from the MVE1785- and MVE1971-corresponding positions of six other flaviviruses, despite low sequence homology in some cases. Notably, anti-MVE1785 Tc cells recognized a determinant (TDGEERVI) which shares with the determinant used for stimulation only the carboxy-terminal amino acid residue, one of two H-2Kk anchor residues. These reactivity patterns were also observed in peptide-dependent interferon-gamma production and the requirements for in vitro restimulation of memory Tc cells. However, the broad cross-reactivity appeared to be limited to flavivirus-derived determinants, as none of a range of determinants from endogenous mouse-derived sequences, similar to the MVE-determinants, were recognized. Neither were cells infected with a number of unrelated viruses recognized. These results raise the paradox that virus-immune Tc cell responses, which are mostly directed against only a few "immunodominant" viral determinants, are remarkably peptide cross-reactive.

Cytotoxic T cell memory
Although T cell memory was first described over fifty years ago much remains to be learned about the biochemical and cellular basis of the phenomenon. We do not have detailed knowledge of the cellular events which lead to the establishment of T cell memory (eg.the probability of an asymetric mitosis model). We are not even able to identify a memory Tc cell phenotype precisely. Most progress has been made in analysing the general functional properties and activation requirements of memory T cells. The availability of a virus model which allows induction of primary Tc cell responses but which does not lead to the generation of long lasting memory Tc cells may prove to be a valuable tool in unravelling further aspects of T cell memory.

 

Viral Immunology Group
Professor R.V. Blanden

The Viral Immunology Group contains a number of laboratories investigating different aspects of fundamental properties of the immune system and viruses. Various projects concern the structure and evolution of the genes that encode antibodies, programmed cell death in relation to viral immune evasion strategies, viral replication processes and immune responses against viral infection.

Immunology Laboratory
Professor RV Blanden

In adult humans, many of the B lymphocytes responsible for memory and secondary antibody responses display mutations in the genes encoding the protein chains of the antibody molecule. These mutations contribute to the phenomenon of affinity maturation of antibody responses in which secondary and later responses show improvement in affinity over early responses, thus improving the protective potential of the antibodies.

Conditions under which hypermutation of antibody genes is induced in B lymphocytes and the mechanisms of selection of B cells with mutated antibodies of high affinity against the immunizing antigen have been well defined. However the molecular mechanism of somatic hypermutation remains one of the major unsolved mysteries in immunology. We are testing an hypothesis involving pre-mRNA from rearranged variable regions of antibody genes as the primary target of sequence variation. Reverse transcription then produces mutated cDNA which replaces the original gene by homologous recombination. Predictions of this molecular model are being tested using transgenic mice.


Experimental Haematology Group (until July)
Dr Andrew J Hapel

The underlying objective of this group is to understand the mechanisms of lineage determination in the haematopoietic system. To achieve this we are studying the molecular mechanisms by which cytokines transmit signals to the nucleus of progenitor cells causing them to proliferate, differentiate or die. We are also interested in how the functions of mature blood cells, particularly macrophages and dendritic cells are regulated. We have developed cellular systems which can be used in vitro to examine the effect of the origin and phenotype of antigen handling cells on immune induction/regulation. Virtually all of our work is done using recombinant cytokines that we make in this laboratory, and cell lines that we derive from yolk sac, fetal liver and adult bone marrow.

In order to generate reliable molecular data it is important to use homogeneous populations of cells. It is difficult to do this by isolating cells ex vivo so emphasis is placed on the generation of cell lines. Our primary experimental system involves the use of cell lines that we have made by transfecting progenitor cells that proliferate in response to granulocyte-macrophage colony-stimulating factor (GM-CSF) with a retrovirus that contains a cDNA encoding a truncated form of c-Myb. Expression of this unregulated c-Myb allows the cells to grow indefinitely in GM-CSF. Expression of Myb is a prerequisite for normal proliferation of myeloid cells. As far as we know our myb-transformed haematopoietic cell lines (MTHC) differ from "normal" cells only in the unregulated expression of myb.

As is the case for many myelomonocytic cell lines we have tested, myb-transformed cell lines grown in GM-CSF can be induced to differentiate into macrophages in the presence of tumour-necrosis factor alpha (TNF-alpha) and interleukin-4 (IL-4), while the use of interferon gamma (IFN-gamma) instead of IL-4 forces the cells into the dendritic cell lineage. We are examining the novel genes that are expressed during commitment to these two different lineages using the technique of cDNA subtraction. The preparation of subtractive libraries was done by Dr. Joanne Banyer, then a post-doctoral fellow in the group. From these libraries we have isolated a large number of genes that are selectively involved in either macrophage and/or dendritic cell differentiation and are now identifying and characterising these genes as a prelude to investigating their role in differentiation and cell function.

Instead of differentiating in response to TNF-alpha some of our cell lines undergo programmed cell death or apoptosis. Since the apoptotic (A) and differentiating (D) cell lines were sub-cloned from the same cultures we are trying to determine the key differences between them that result in such different outcomes of TNF-alpha signaling. During her thesis work in this group Peta O'Connell showed that one difference between the A and D cells was that when apoptosis occurred it did so as a result of ligand binding to both type I and type II TNF receptors whereas differentiation required binding to the type I receptor only. Another student, Mr. Hayden Henry, attempted to identify differences in the signaling pathways downstream from the receptors, and in collaboration with Dr. Banyer identified several genes that are selectively expressed or silenced in the A vs D cell lines.

At the level of cell biology we have shown that macrophages that differentiate in vitro from myb transformed cell lines are effective at phagocytosis but are poor presenters of antigen. In contrast, cells of the dendritic phenotype, induced by IFN-gamma, have potent antigen presenting capacity. In an attempt to induce immune responses against tumour antigens we are transfecting selected genes into our progenitor cell lines and inducing differentiation with cytokines. Differentiated cells can then be used to immunise mice or to induce immune responses in vitro. This cell system provides a model for examining antigen processing and presentation, and for identifying phenotypic differences between antigen handling cells that influence immune class regulation.

Another program of work involves the application of gene targeting technology toward the analysis of certain aspects of cytokine signaling. We have made targeting constructs designed to knock out the receptor for M-CSF (c-fms) and the alpha chain of the interleukin-3 receptor. By combining gene targeting technology with the construction of myb-transformed cells lines from targeted ES cells, we can potentially circumvent the need for viable knock out mouse strains should any of these induced mutations prove lethal in the whole animal. As we identify and learn more about the genes that are involved in apoptosis, proliferation and differentiation of myeloid cells we will use targeting technologies to identify the biological role of targeted genes in vivo.

The group is now located in the Research School of Chemistry and is funded entirely by Glaxo Wellcome.

 

Staff - Division of Immunology and Cell Biology

Professor and Head:
CR Parish, BAgrSc (Melb), PhD (Melb)

School Technical Manager: (until June)
J Bateman, BSc (Syd) (until June)
School Technical Support Officer: (from June)
CE Woodhams, BAppSc (CCAE), GradDipInfSyst (Canb) (from June)
Senior Technical Officer: (until June)
CE Woodhams, BAppSc (CCAE), GradDipInfSyst (Canb) (until June)
Division Adminstrator: ETF Weil
Administrative Assistant: M Anderson (part-time)

Cell-Cell Interaction Group
Professor and Leader:
CR Parish, BAgrSc (Melb), PhD (Melb)
Fellow (N-C): (externally funded)
WB Cowden, BSc (Troy State), PhD (Qld) (fractional)
Fellow: (externally funded)
C Freeman, BSc (Hons) (Adel), PhD (Adel) (from July)
Research Fellow: (externally funded)
C Freeman, BSc (Hons) (Adel), PhD (Adel) (until July)

M Hulett, BSc (Hons) (Melb.) PhD (Melb.) (from July)
Postdoctoral Fellow:
 M Hulett, BSc (Hons) (Melb.) PhD (Melb.) (until July)
Postdoctoral Fellows: (externally funded)
KJ Brown, BSc (Hons), PhD (until August);
VM Cabalda-Crane, BSc (Univ.Santo Tomas, Manila), PhD (Birmingham, UK);
J McHenry, BSc (Hons) (Victoria University,Wellington), PhD (until March)
Visiting Fellows:
BJ Allen, BSc (Melb), MSc (Melb), PhD (Wollongong), DSc (Melb) (until April); J Altin, BSc, GradDipSci, PhD; NA Bowern, MPhil (Brunel), PhD; KJ Brown, BSc (Hons), PhD (from August); C Chesterman, MBBS (Syd), D.Phil (Oxf), FRACP, FRCPA; G Chong, MBBS (Hons), BMedSc (Monash) FRACS, FRCS (C) FRCS (E), Diplomate, American Board of Surgery (USA); IA Clark, BVSc (Qld), PhD (Lond), DSc (Lond); D Francis, BVSc (Syd), MVSc (Syd), PhD (Syd); M Staykova, PhD (Univ of the Sofia, Bulgaria); RD Simmons, BBSc (Hons), PhD (La Trobe); H Warren, BSc (Hons), PhD (Qld); DO Willenborg, BSc (Illinois), MSc (Calif), ScD (Johns Hopkins)
Research Scientists: (externally funded)
S Gerba, BSc, MSc (Addis Ababa University, Ethiopia), PhD; B Eschler, BSc(Hons) (Syd), Dip.Ed. (Syd), MSc (Syd), PhD (Wollongong) (from January)
Research Associate:
J Wang, BSc (Hebei), PhD (from April)
Research Assistant: (externally funded)
M Philippa, BSc, MPhil (Griffith) (until December)
Senior Technical Officers:
KB Jakobsen, DVM (Copenhagen); J. Hornby, BSc (Hons) (Queens, Belfast)
Senior Technical Officer: (externally funded)
A Bezos, BSc (Syd) MSc (Syd)
Technical Officers: (externally funded)
A Browne, BA; JP Gapella, Animal Tech Cert (TAFE); G Bartell, BSc (Hons) (Syd); V McPhun, MSc (Lond) Technical Officer: E Pagler, BS (Med.Tech Univ Santo Tomas, Philippines) Laboratory Technician: (externally funded)
L Geale, DipAppSciAnimalTechnology (CIT) (from April - November)
Administrator (externally funded): P Basnett (part-time)

 

Viral Immunology Group


Professor and Leader
RV Blanden, MDS (Adel), PhD, FAA

Immunology Laboratory
Professor and Leader:
RV Blanden, MDS (Adel), PhD, FAA
Postdoctoral Fellows:
C Bruce, BSc (Hons) (Reading), PhD (Reading) (until June);
K. Kellaher, BSc(Hons) (UWA), PhD (from August-November part-time)
Visiting Fellows: GL Ada, DSc (Syd) FAA; D Cohen, BSc (Hons) (Syd), PhD; P.D. Cooper, DSc, PhD (Lond); A Gautam, BSc (Meerut), MSc (Brunel), PhD (Lond); E.J. Steele, BSc (Hons) (Adel), PhD (Adel)
Technical Officer: P Boyce, PostGrad Cert. DNA Tech. (CIT)

 

Apoptosis Laboratory (until December)
Fellow (N-C) and Leader:
P Waring, BSc (Hons) (Qld), MSc, PhD (until December)
Laboratory Technician:
T Davis, Ass.Dip.Tech.Biol.(CIT) (until November)

Molecular Virology Laboratory
Fellow (RFT) and Leader:
M Lobigs, BSc (Hons), PhD
Research Fellow:
E Lee, BSc (Hons), PhD (from July-November)
Postdoctoral Fellow:
E Lee, BSc (Hons), PhD (until July)
Technical Officer:
M Pavy, Ass.Dip.AppSc (CIT)

Molecular Immunology and Immunopathology Group
Senior Fellow and Leader:
A Müllbacher, BSc, MSc (Auck), PhD
Research Fellow:
E Lee, BSc (Hons), PhD (from November)
Postdoctoral Fellow:
I Ferru, PhD (Pasteur Institute) (until August)
Visiting Fellows:
ML Bassett, MB ChB (Otago), MD (Qld), FRACP (from October); J Chin, MSc (Hons) (Qld), PhD (Qld); R.B. Ashman, BSc (Hons)(WA), PhD (WA), DSc (WA) ; I Ferru, PhD (Pasteur Institute) (from August)
Senior Technical Officer:
R Tha Hla, BRTC (TAFE)
Technical Officer: S Chin, B.Tech (UK) (until June)

Viral Engineering and Cytokine Research Group:
Professor and Leader:
IA Ramshaw, MSc (Brunel), PhD
Research Fellow: (externally funded)
S Thomson, BSc (Syd), PhD (Qld)
Postdoctoral Fellows:
J Banyer, BSc (Hons) (Griffith), PhD; S Prasad BSc(Hons) (AWU), PhD (from April)
Visiting Fellows:
RJ Jackson, BSc (Hons) (Monash), PhD (Edin); A Ramsay, BSc, PhD (Otago)
Senior Technical Officer:
CJ Medveczky, AssocDipTechBiol (TAFE)
Technical Officers: (externally funded)
M Shoobridge, BSc (Hons); B. Matheson, BTC (TAFE ), BSc (from September)
Technical Officers:
T Sutherland, BappSc (Charles Sturt Uni) (from February-October); T Davis, Ass.Dip.Tech.Biol.(CIT) (from November)
Laboratory Technicians: (externally funded)
A Wheatley BSc (Hons) (from July); A Murfett, BAppSciBiotech (QUT) (from July-December)

Experimental Haematology Group (until July)
Senior Fellow and Leader:
A Hapel, BSc (Hons) (NELU), PhD (until July)
Postdoctoral Fellow: J Bettadapura ,BSc, MSc (Mysore University, India), PhD (Indian Institute of Science, Bangalore) (from February - July); W Gu, MSc (North Eastern Agricultural University, Harbin, China) (from February - July)
Visiting Fellow:
B Lidbury, BSc (Hons) (Newcastle), PhD (until July)
Senior Technical Officer: J Olsen, BSc (until July)