ARDC Research Link Australia Research Link Australia   BETA Research
Link
Australia
  • ARDC Newsletter Subscribe
  • Contact Us
  • Home
  • About
  • Feedback
  • Explore Collaborations
  • Researcher
  • Funded Activity
  • Organisation
  • Researcher
  • Funded Activity
  • Organisation
  • Researcher
  • Funded Activity
  • Organisation

Need help searching? View our Search Guide.

Advanced Search

Current Selection
Scheme : NHMRC Project Grants
Research Topic : Interfeon modulation
Status : Closed
Clear All
Filter by Field of Research
Medical Virology (4)
Medical biotechnology diagnostics (incl. biosensors) (2)
Anaesthesiology (1)
Cell Metabolism (1)
Clinical chemistry (incl. diagnostics) (1)
Clinical sciences not elsewhere classified (1)
Medical biochemistry and metabolomics not elsewhere classified (1)
Nutritional science (1)
Pharmacology and Pharmaceutical Sciences (1)
Radiotherapy And Nuclear Medicine (1)
Signal Transduction (1)
Filter by Socio-Economic Objective
Search did not return any results.
Filter by Funding Provider
National Health and Medical Research Council (20)
Filter by Status
Closed (20)
Filter by Scheme
NHMRC Project Grants (20)
Filter by Country
Search did not return any results.
Filter by Australian State/Territory
Search did not return any results.
  • Researchers (0)
  • Funded Activities (20)
  • Organisations (0)
  • Funded Activity

    How Do Flaviviruses Modulate Interferon Response

    Funder
    National Health and Medical Research Council
    Funding Amount
    $457,500.00
    Summary
    Several members of the Flaviviridae family are major pathogens of humans including dengue (DEN), yellow fever (YF), tick-borne encephalitis (TBE), Murray valley encephalitis (MVE), Japanese encephalitis (JE), and hepatitis C virus (HCV). An Australian flavivirus Kunjin (KUN), however, appears to be naturally attenuated and does not cause an overt disease in humans. In contrast, genetically and antigenically closely related to KUN, New York strain of West Nile virus (NY WN) has already caused ~50 .... Several members of the Flaviviridae family are major pathogens of humans including dengue (DEN), yellow fever (YF), tick-borne encephalitis (TBE), Murray valley encephalitis (MVE), Japanese encephalitis (JE), and hepatitis C virus (HCV). An Australian flavivirus Kunjin (KUN), however, appears to be naturally attenuated and does not cause an overt disease in humans. In contrast, genetically and antigenically closely related to KUN, New York strain of West Nile virus (NY WN) has already caused ~500 deaths and over 20,000 registered infections since its emergence in North America in 1999, including 223 deaths and 9122 infections in 2003 alone. Recent studies with DEN indicated that flaviviruses may interfere with early steps of IFN-signalling pathway. The type I Interferon (IFN) response is the first line of defence against viral infections and many viruses have developed different strategies to counteract this response in order to ensure their survival in the infected host. In this grant we seek to exploit our extensive understanding of the molecular biology of KUN virus and the contrasting behaviour of KUN and NY WN viruses to gain an understanding of the role of flavivirus-mediated suppression of host anti-viral IFN response in virus-host relationships and its importance in determining virus virulence.
    Read more Read less
    More information
    Funded Activity

    Probes For The Modulatory Site Of The Nicotinic Recepto R

    Funder
    National Health and Medical Research Council
    Funding Amount
    $278,207.00
    More information
    Funded Activity

    Cellular Microenvironments Facilitating The Replication And Propagation Of Flaviviruses

    Funder
    National Health and Medical Research Council
    Funding Amount
    $505,279.00
    Summary
    Flaviviruses are the agents of many mosquito-transmitted infections and many deaths globally each year. The emerging virus West Nile virus (strain New York) is a member of this virus family and shares 99% amino acid homology with the endemic Australian virus Kunjin virus. During virus growth in cells, cellular membrane structures are induced or rearranged by these viruses for their own purpose. That being the production of more virus particles for reinfection of other cells. Using Kunjin virus a .... Flaviviruses are the agents of many mosquito-transmitted infections and many deaths globally each year. The emerging virus West Nile virus (strain New York) is a member of this virus family and shares 99% amino acid homology with the endemic Australian virus Kunjin virus. During virus growth in cells, cellular membrane structures are induced or rearranged by these viruses for their own purpose. That being the production of more virus particles for reinfection of other cells. Using Kunjin virus as a model, and advanced techniques in biochemistry and electron microscopy, we have identified for the first time these membrane structures as the apparent sites of replication of the viral RNA or genetic material, and of the viral proteins involved. We have also observed how new virus particles are able to get out of infected cells and shown how some drugs can prevent this occurring thus limiting their transmission. This research will focus on how the membrane structures are formed in infected cells. The research will determine what cellular components are required by the virus to help it propagate. In particular specific cellular proteins and membrane components that are captured by the virus and moved to different sites in the infected cells. These apparent requirements could possibly lead us to a greater understanding of the complex interactions that occur between the invading virus and the host cells. We aim to directly visualize the process of infection within living cells using new and innovative microscopic techniques. Another of our objectives is to determine the effects of infection on normal cells. The question being whether flavivirus infection disrupts normalcell fuctions like secretion etc. An understanding of these processes, and how the viral RNA is copied into new RNA for more virus particles, will assist in the development of antiviral drugs for treatment of this pathogenic group of viruses.
    Read more Read less
    More information
    Funded Activity

    Repair Of The Stomach Lining After It Is Damaged: How C An We Assist It?

    Funder
    National Health and Medical Research Council
    Funding Amount
    $100,202.00
    More information
    Funded Activity

    Regulation Of The Effects Of Nerve Injury Or Limb Amput Ation On Brain Pathways

    Funder
    National Health and Medical Research Council
    Funding Amount
    $896,887.00
    More information
    Funded Activity

    Neurotransmitter Modulation Of Striatial And Hypothalmi C Neurons

    Funder
    National Health and Medical Research Council
    Funding Amount
    $296,587.00
    More information
    Funded Activity

    Looking For Ways To Supplement Improve Present Treatments For Arthritis

    Funder
    National Health and Medical Research Council
    Funding Amount
    $240,842.00
    More information
    Funded Activity

    Modulation Of Apoptosis By Cytomegalovirus: Analysis Of New Mechanisms To Interfere With Cytomegalovirus-induced Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $697,084.00
    Summary
    Apoptosis, or programmed cell death is an essential process in developmental and homeostatic control of complex biological systems. In addition to these primary house keeping roles, apoptosis provides a powerful defence mechanism against invading pathogens, such as viruses, since it allows early elimination of infected cells from the host. A basic property of herpesviruses is their ability to establish persistent infection and remain in association with the host for its lifetime. This strongly u .... Apoptosis, or programmed cell death is an essential process in developmental and homeostatic control of complex biological systems. In addition to these primary house keeping roles, apoptosis provides a powerful defence mechanism against invading pathogens, such as viruses, since it allows early elimination of infected cells from the host. A basic property of herpesviruses is their ability to establish persistent infection and remain in association with the host for its lifetime. This strongly underlines their success at reaching an accommodation with the immune system's anti-apoptotic mechanisms. The central hypothesis of this project is that herpesviruses, such as murine and human cytomegalovirus, encode proteins that interfere with cell death pathways thereby circumventing host defence so that viral replication and dissemination can proceed. Thus, the aims are to identify and characterise cytomegalovirus proteins that modulate apoptosis. These studies will improve our understanding of the control of apoptosis during viral infection, especially as caused by cytomegaloviruses. Human cytomegalovirus (HCMV) is a pathogen able to cause significant morbidity and mortality in individuals with immature or compromised immune systems, such as newborns, AIDS patients, transplant recipients and people treated with chemotherapeutic drugs. Hence, the proposed studies will allow the elucidation of molecular mechanisms that may be relevant to the pathogenesis of HCMV in man and will provide insights into the rational design of suitable antiviral drugs and vaccines. Understanding viral mechanisms of host immune evasion continues to improve our understanding of complex cellular pathways. Therefore, given that abnormal regulation of apoptosis is implicated in the development of degenerative conditions, cancer and autoimmune disease, the proposed studies will provide valuable insight towards the development of new therapies for these pathological conditions.
    Read more Read less
    More information
    Funded Activity

    Positive Modulation Of Ionotropic GABA Receptors

    Funder
    National Health and Medical Research Council
    Funding Amount
    $540,023.00
    Summary
    Substances that enhance the action of the inhibitory neurotransmitter GABA in the brain are amongst the most widely used drugs. They include many anaesthetics, anxiolytics and sedatives. Their enhancing action is mediated by increasing the effectiveness of GABA acting on GABA receptors, in particular the subtype of GABA receptors known as GABA-A receptors. This action, termed positive modulation, is poorly understood in molecular terms. Our discovery of second order modulators that only act in c .... Substances that enhance the action of the inhibitory neurotransmitter GABA in the brain are amongst the most widely used drugs. They include many anaesthetics, anxiolytics and sedatives. Their enhancing action is mediated by increasing the effectiveness of GABA acting on GABA receptors, in particular the subtype of GABA receptors known as GABA-A receptors. This action, termed positive modulation, is poorly understood in molecular terms. Our discovery of second order modulators that only act in conjunction with first order modulators adds an exciting new dimension to the concept of influencing the ways in which GABA receptors can be modulated. This offers a new approach to the development of therapeutic agents acting on GABA receptors and thus the treatement of important disorders such as anxiety, epilepsy and insomnia.
    Read more Read less
    More information
    Funded Activity

    Molecular Anatomy Of Radiation Hypersensitivity

    Funder
    National Health and Medical Research Council
    Funding Amount
    $392,545.00
    Summary
    Radiotherapy (RT) is a curative anti-cancer treatment employed in around half of all cancer sufferers. Very occasionally, a cancer patient will manifest an unexpected adverse reaction to RT and there is strong evidence for a genetic basis to such RT sensitivity. Despite two decades of research, such reactions cannot currently be predicted prior to treatment and their occurrence limits the intensity, and hence cure rates, of RT for the majority of patients. This project will employ cutting edge t .... Radiotherapy (RT) is a curative anti-cancer treatment employed in around half of all cancer sufferers. Very occasionally, a cancer patient will manifest an unexpected adverse reaction to RT and there is strong evidence for a genetic basis to such RT sensitivity. Despite two decades of research, such reactions cannot currently be predicted prior to treatment and their occurrence limits the intensity, and hence cure rates, of RT for the majority of patients. This project will employ cutting edge technology (DNA Chips, or microarrays) to attempt to understand why some patients suffer significant RT side-effects, while the vast majority do not. We have developed a tissue bank of samples from cancer patients who have had adverse RT reactions, and these samples (and samples from unaffected cancer patients) will be examined by microarrays: the activity of thousands of genes will be evaluated in each experiment, and we shall search for patterns of gene activity which track with RT sensitivity. Should we determine a pattern, this pattern will be checked against a larger number of cases and if it accurately predicts RT sensitivity, could lead to the routine testing of cancer patients prior to RT and the individualisation of cancer therapy. In parallel, we will evaluate the tissues of sensitive patients with assays capable of detecting abnormalities in the response to radiation, which may give clues as to an underlying gene fault(s) which might predispose to radiosensitivity in that individual.
    Read more Read less
    More information

    Showing 1-10 of 20 Funded Activites

    • 1
    • 2
    Advanced Search

    Advanced search on the Researcher index.

    Advanced search on the Funded Activity index.

    Advanced search on the Organisation index.

    National Collaborative Research Infrastructure Strategy

    The Australian Research Data Commons is enabled by NCRIS.

    ARDC CONNECT NEWSLETTER

    Subscribe to the ARDC Connect Newsletter to keep up-to-date with the latest digital research news, events, resources, career opportunities and more.

    Subscribe

    Quick Links

    • Home
    • About Research Link Australia
    • Product Roadmap
    • Documentation
    • Disclaimer
    • Contact ARDC

    We acknowledge and celebrate the First Australians on whose traditional lands we live and work, and we pay our respects to Elders past, present and emerging.

    Copyright © ARDC. ACN 633 798 857 Terms and Conditions Privacy Policy Accessibility Statement
    Top
    Quick Feedback