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Research Topic : Replication fitness
Country : Australia
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Medical Virology (4)
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  • Funded Activity

    Life On Holidays: Fitness Lost, Fatness Regained?

    Funder
    National Health and Medical Research Council
    Funding Amount
    $880,685.00
    Summary
    There’s recent evidence that children get leaner and fitter during the school term, but become fatter and less fit over the summer holidays. This may be because of differences in activity and diet: on holidays, children may eat more, be less active and have more screen time. We propose to track the time use, diet, fitness and fatness of 9-11 year old children across three school years. If the pattern is confirmed, we should focus more on the home environment, or perhaps encourage summer camps.
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    Funded Activity

    A Scalable Intervention For Increasing Vigorous Physical Activity Among Older Adolescents: The ‘ Burn To Learn ’ Cluster RCT

    Funder
    National Health and Medical Research Council
    Funding Amount
    $636,912.00
    Summary
    Physical inactivity has been described as a global pandemic and only 15% of Australian adolescents are sufficiently active. The pressure to perform in major school assessments drives many older adolescents to sacrifice physical activity to maximise academic performance. Our team has designed a time-efficient solution to increase physical activity in senior high school students using high intensity interval training which will be evaluated using a cluster randomised controlled trial.
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    Research Fellowship - Grant ID:425513

    Funder
    National Health and Medical Research Council
    Funding Amount
    $559,560.00
    Summary
    I am a physiotherapist with special expertise in ergonomics. My research aims to improve health outcomes through an understanding the physical impact of new technology use.
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    Mechanisms Underlying APOBEC3G Restriction Of HIV-1

    Funder
    National Health and Medical Research Council
    Funding Amount
    $540,075.00
    Summary
    In the fight against worldwide HIV-AIDS, understanding natural cell defenses to the HIV virus may identify new virus targets and strategies to block HIV in humans. Here, we will use state-of-the-art, high resolution, fluorescent microscopy to understand how the recently identified cell protein, APOBEC3G, blocks the HIV life cycle in human cells. We anticipate that APOBEC3G will stop HIV from invading the nucleus of human cells to defend against HIV, a strategy we can apply to new therapies.
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    How Replication Stress Activates The Mitotic Telomere DNA Damage Response To Kill Cancer Cells

    Funder
    National Health and Medical Research Council
    Funding Amount
    $486,467.00
    Summary
    We discovered a novel mechanism linking stress during DNA replication to difficulties with the cell division process, and identified how this turns on DNA damage response signals from the chromosome ends (i.e. “telomeres”). We have further identified that we can exploit this mechanism to kill cancer cells. In this project we will explore this newly discovered mechanism and identify how it can be targeted for therapeutic purposes.
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    Funded Activity

    Norovirus Infection At The Stress Granule-PKR-p-elF2α Axis

    Funder
    National Health and Medical Research Council
    Funding Amount
    $505,967.00
    Summary
    This project application will aim to investigate and understand how viruses that cause vomiting and diarrhoea are able to infect, proliferate and spread within the human body. It aims to address how viruses are able to avoid and replicate in the presence of an effective immune response. We have evidence showing that Noroviruses are able to exploit certain antiviral proteins to paradoxically aid in virus replication and survival.
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    Funded Activity

    Uncoupled Research Fellowship

    Funder
    National Health and Medical Research Council
    Funding Amount
    $715,611.00
    Summary
    I am a molecular virologist researching the host response to hepatitis C virus (HCV) infection with the aim of understanding how the liver clears HCV infection. An understanding of this process will hopefully lead to novel antiviral strategies to combat not only HCV but a broad range of other viral infections.
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    Funded Activity

    The Mechanism Of HSV-1 Transport In Sensory Axons And Its Unique Assembly At The Axon Terminus

    Funder
    National Health and Medical Research Council
    Funding Amount
    $670,284.00
    Summary
    Herpes simplex viruses 1 and 2 cause common diseases such as genital herpes and, occasionally, neonatal deaths and encephalitis and predisposes to HIV infection. New antiviral strategies are required for resistant viruses for control. These aims will be facilitated by understanding how HSV is transported down nerves and across into skin. In this study, we will define how a key viral protein plays a major role in assembly of the virus at the tip of the nerve before it enters skin.
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    Funded Activity

    Molecular Studies Of The Astrocyte Reservoir Of HIV-1 In The Central Nervous System

    Funder
    National Health and Medical Research Council
    Funding Amount
    $592,661.00
    Summary
    HIV infects the brain causing dementia in 10-20% patients. Strategies aimed at eradicating HIV infection fail to take into account CNS infection. Understanding the way in which HIV enters, infects and replicates in the brain is pivotal in development of drugs to prevent brain infection and dementia. Our studies have shown that HIV infection of the brain involves mechanisms distinct to those observed for blood and other organs. This study seeks to clarify such mechanisms.
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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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