Understanding The Innate Immune Response To Viral Infection Of The Female Reproductive Tract And Placenta
Funder
National Health and Medical Research Council
Funding Amount
$784,273.00
Summary
Viral infection of the female reproductive tract (FRT) can have a significant impact on FRT health and may cause significant birth defects if the virus infects the placenta and developing fetus. In this application we will investigate the role of a novel molecule termed interferon epsilon and how it impacts viral infection of the FRT, the fetus and how the placenta responds to viral infection. This work will develop innovative antiviral strategies to combat viral infections of the FRT.
Amyotrophic Lateral Sclerosis (ALS) is a progressively fatal neurodegenerative disease characterized by aggregates of a protein called TDP-43. ALS also features the presence of several inflammatory cytokines in the central nervous system. In this project, we will study how TDP-43 abnormally mislocalizes within cells, releasing mitochondrial DNA and triggering a novel pathway of inflammation. We propose that targeting this pathway could lead to new treatments for ALS.
Interferon Epsilon As A Novel Regulator Of Host-bacterial Interaction In Homeostasis, Infection And Inflammation
Funder
National Health and Medical Research Council
Funding Amount
$843,088.00
Summary
Gut infections are a leading cause of death worldwide and healthcare use in Australia. Inflammatory bowel disease (IBD) is incurable and affects 1/200 young Australians. Type I interferons (T1IFNs) are important to control gut infections and IBD by interacting with particular bacterial species in the gut. We discovered one T1IFN, IFNε, in human gut. It protects against models of IBD in mice. We will use mouse and human samples to find bacterial or interferon treatments for infections and/or IBD.
Vascular Changes Are A Key Contributor To And Novel Drug Target For Interferon-alpha Induced Neurological Disease
Funder
National Health and Medical Research Council
Funding Amount
$1,245,401.00
Summary
Type I interferons (IFN-Is) contribute to wide range of neurological diseases including ageing and neurodegeneration. At its extreme IFN-I-mediated neurodegeneration is known as 'interferonopathy'. The mechanisms of how IFN-Is drive disease are unclear, making causal treatment difficult. We have recently uncovered ground-breaking evidence that abnormal blood vessels are a key contributor to the disease. Here, we will investigate novel treatment targets for patients with interferonopathies.