The Host Response To Highly Pathogenic Influenza Virus
Funder
National Health and Medical Research Council
Funding Amount
$237,981.00
Summary
Highly pathogenic influenza infections are a global health concern and cause global panic. There is no effective therapy available; for example and the death rate for H5N1 infection is ~60%. Here we propose to further understand host lung response to highly pathogenic influenza with a view to develop new therapies for this urgent issue.
Discovery Early Career Researcher Award - Grant ID: DE130100470
Funder
Australian Research Council
Funding Amount
$375,000.00
Summary
Understanding mechanisms and functions of evolutionary divergence in innate immune genes. Microorganisms constantly challenge the immune systems of all multi-cellular organisms, and host immune genes must be able to co-evolve with microbes in order for a species to propagate. This project will investigate how host immune genes in a species evolve to enable that species to continue.
Why do neutrophils swarm? This project aims to combine novel immunology, microscopy and computational approaches to investigate how immune cells called neutrophils cooperate to protect the host against microbes. Neutrophils are rapidly recruited to sites of inflammation and then utilise a type of highly coordinated collective behaviour termed swarming. However, the role of neutrophil swarms in fighting off infection is poorly understood. The project is poised to generate new knowledge on the imp ....Why do neutrophils swarm? This project aims to combine novel immunology, microscopy and computational approaches to investigate how immune cells called neutrophils cooperate to protect the host against microbes. Neutrophils are rapidly recruited to sites of inflammation and then utilise a type of highly coordinated collective behaviour termed swarming. However, the role of neutrophil swarms in fighting off infection is poorly understood. The project is poised to generate new knowledge on the importance of immune cell cooperation by developing in silico models of the immune response. The project will provide benefit through enhanced understanding of fundamental principles of immunity and develop new computational tools to model complex immune function in silico.Read moreRead less
Innate Immune Functions Of The Intracellular Antibody Receptor TRIM21
Funder
National Health and Medical Research Council
Funding Amount
$408,768.00
Summary
The immune system can fight viral infections with antibodies, which mark viruses outside of cells for elimination by immune cells. Antibody-coated viruses try to escape elimination by hiding inside cells. This project will determine how immune cells recognise the antibody-coated viruses ‘hiding’ within them, and the defence response they launch to eliminate viral infection. Such knowledge may allow us to develop better anti-viral drugs and vaccines to fight viral diseases like the common cold.
The Role Of IL-17 In Regulating Liver Macrophage Permissiveness For Leishmania Infection
Funder
National Health and Medical Research Council
Funding Amount
$655,082.00
Summary
Visceral Leishmaniasis is a disease of poverty in the developing world caused by Leishmania parasites, which live and replicate within host tissue macrophages. A cytokine produced by host cells, IL-17A impairs the ability of liver macrophages to control this infection, as mice that lack IL-17A have lower parasite burdens in the liver after experimental infection. We propose to investigate if IL-17A mediates this impaired control by tuning the permissiveness of host macrophages to infection.
Combating Infectious Diseases By Harnessing Macrophage Functions
Funder
National Health and Medical Research Council
Funding Amount
$688,152.00
Summary
Infectious diseases present a persistent global health threat. For patients with life-threatening diseases caused by bacterial pathogens, antibiotics provide the last resort. Antibiotic resistance, even for newly developed antibiotics, is widespread within the bacterial community. New strategies are urgently needed to combat most bacterial infections. This proposal will investigate a new strategy to train and boost our immune systems to combat infectious diseases.
The Role Of A Novel Cytokine Of The Innate Immune Response In Viral Infection
Funder
National Health and Medical Research Council
Funding Amount
$344,407.00
Summary
Sexually transmitted infections represent a critical global health and socioeconomic problem with over 1 billion new cases per annum. I propose a world-first description of a new protein that has a protective role against herpes simplex virus (HSV) infection of female reproductive tract. This unique protein, called interferon epsilon, was discovered in our laboratory. This project will facilitate development of new therapeutic approaches of benefit in HSV-2 infection.
Elucidating The Critical Roles Of ILC1, NK Cell And Innate Memory In Immune Protection
Funder
National Health and Medical Research Council
Funding Amount
$657,024.00
Summary
Natural killer cells are innate cells that provide first line defense against infection and cancer. The recent discovery of a novel innate cell population has modified our vision of the early events necessary for immune protection. Understanding the role of these cells is critical as they could represent viable therapeutic targets. We have developed unique mouse models to experimentally target this population to determine how they are generated and their role in combating infection and cancer.
As the first recruited cells, neutrophils direct protective responses against infection, but can also mediate destructive responses in inflammatory disease. This project will determine mechanisms driving neutrophil-dependent inflammation in both settings, by examining a specific inflammation-promoting molecular pathway (the ïinflammasomeÍ) in neutrophils. This research will lead to a better understanding of inflammation, and may suggest therapeutics for treating inflammatory disease.
PB1-F2 Is Critical To Influenza A Virus Pathogenicity Through Activation Of The Inflammasome
Funder
National Health and Medical Research Council
Funding Amount
$663,919.00
Summary
Fatal Influenza A virus infections are excessive inflammation. We identified the IAV protein PB1-F2 as critical in driving excessive inflammation via activating the host inflammasome complex. Our study evaluates PB1-F2-mediated inflammation contribution to inflammatory responses. Identifying PB1-F2 in emerging IAV strains is invaluable in aiding health policy makers to quickly assess fatal IAV pandemics. Our research will potentially identify treatment targets towards reducing this inflammation