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Field of Research : Infectious Diseases
Research Topic : Viral glycoprotein function
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  • Funded Activity

    Detection And Clinical Significance Of Human Cytomegalovirus (CMV) Specific T Cell Immunity Following Transplantation

    Funder
    National Health and Medical Research Council
    Funding Amount
    $139,556.00
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    Funded Activity

    Practitioner Fellowship

    Funder
    National Health and Medical Research Council
    Funding Amount
    $408,302.00
    Summary
    I am an infectious diseases physician and basic scientist interested in the immunopathogenesis of HIV and hepatitis B virus. My work focuses on HIV viral reservoirs and immune reconstitution and the adaptive immune response to hepatitis B virus.
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    Funded Activity

    Genomic Analysis Of Host Response To Influenza A Infection

    Funder
    National Health and Medical Research Council
    Funding Amount
    $168,530.00
    Summary
    Influenza virus infects millions of people globally. However, it remains poorly understood why some infected individuals succumb to life threatening complications whilst others recovered relatively unaffected. This study use advance molecular technique to study influenza infection. It aims to identify the key steps in our immune systems that are progressively disrupted during influenza infection and how this process lead to a break down in our natural defence against the virus.
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    Funded Activity

    A NOVEL MOUSE MODEL TO INVESTIGATE THE MECHANISMS OF VIRUS-INDUCED ARTHRITIS

    Funder
    National Health and Medical Research Council
    Funding Amount
    $336,000.00
    Summary
    We have developed a novel animal model by which to study arthritic disease caused by insect-transmitted viruses known as arboviruses. The existence of this model and novel reagents provides an excellent opportunity to further explore the basic mechanisms of infectious disease in a complete functioning animal, rather than specific cultured cells. The study will use modern approaches in molecular and cellular biology to achieve this goal. The production by our immune systems of soluble mediators ( .... We have developed a novel animal model by which to study arthritic disease caused by insect-transmitted viruses known as arboviruses. The existence of this model and novel reagents provides an excellent opportunity to further explore the basic mechanisms of infectious disease in a complete functioning animal, rather than specific cultured cells. The study will use modern approaches in molecular and cellular biology to achieve this goal. The production by our immune systems of soluble mediators (cytokines-chemokines) and antibodies is an overwhelming positive aspect of our physiological response to infection by microbes. Protection from disease by these immune compounds can happen naturally, or the body's ability to produce these factors can be exploited to our benefit via the administration of vaccines. However, these factors can also be detrimental to the host contributing to severe disease. For instance, work performed almost 40 years ago showed for the first time that under particular conditions, antibodies against viruses can enhance infection, instead of inhibiting infection as normally seen. In the intervening years work by scientists all over the world has associated antibody-dependent enhancement (ADE) of infection to many types of viruses; ADE is even thought to be a risk factor to serious disease with dengue virus, and has been shown in vitro for the AIDS virus and Ebola virus. We have recently discovered a molecular mechanism which explains how antibody enhances viral infection in vitro. In studies on immune cells infected with Ross River Virus (RRV) we found that infection helped by antibody resulted in the specific disruption to the production of cellular chemicals which are toxic to viruses. Are these mechanisms of antibody-enhanced infection also found in animals? Will such mode of infection cause enhanced disease and tissue pathology (arthritis) in animals?
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    Funded Activity

    Trageted Manipulation Of Host Genes And Signalling Pathways To Promote Immune Clearance Of Chronic Viral Infections

    Funder
    National Health and Medical Research Council
    Funding Amount
    $394,460.00
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    Funded Activity

    Study Of Papillomavirus DNA Encapsidation And Formation Of Infectious Virions

    Funder
    National Health and Medical Research Council
    Funding Amount
    $214,053.00
    Summary
    Papillomavirus (PV) is a sexually-transmitted virus that is a major cause of cervical cancer. Our study will determine how PV is able to form new virus particles inside infected cells. This is a critical part of the virus life-cycle, and a better understanding of this process may allow it to be trageted by anti-viral treatments. In addition, we will develop a method to create non-harmful virus particles which we will use to study human immune responses to the virus.
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    Funded Activity

    Immunological Changes During Pregnancy And The Impact On Viral Hepatitis Infection

    Funder
    National Health and Medical Research Council
    Funding Amount
    $353,355.00
    Summary
    Hepatitis B virus (HBV) can cause long term health problems particularly affecting the liver and can be passed from mother to baby. Despite the availability of a HBV vaccine babies can still become infected. During pregnancy there are changes in a woman’s immune system which may impact on HBV infection and make transmission to the baby more likely. This research aims to explore the changes in a woman’s immune system and the impact this has on risks for hepatitis and transmission to the baby.
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    Funded Activity

    Virus-host Balance And Pathogenesis In Persistent Infection

    Funder
    National Health and Medical Research Council
    Funding Amount
    $219,837.00
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    Funded Activity

    Interaction Of Anti-viral IDO And NOS2 In Vivo In A Novel Murine STD Model.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $573,629.00
    Summary
    Sexually transmitted viral diseases (STD) are increasing globally, but we know little of how virus is controlled early in infection. We have shown for the first time in vivo, in our STD model, that during an antiviral immune response, soluble factors turn on an enzyme, indoleamine 2,3-dioxygenase (IDO), to break down and deplete the amino acid, L-tryptophan, starving virus to reduce growth early in STDs. Our project will further define the action and control of IDO in STD.
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    Funded Activity

    The Role Of Histone Deacetylases In Maintenance Of HIV-1 Latency

    Funder
    National Health and Medical Research Council
    Funding Amount
    $96,568.00
    More information

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