Host Metabolism And Responses Contributing To Flavivirus Replication And Pathogenesis
Funder
National Health and Medical Research Council
Funding Amount
$592,772.00
Summary
We aim to determine how viruses affect the cells they infect, In particular how they can alter the metabolism and balance of lipids in cells and how this impacts the bodies capability to respond immunologically. We believe that by understanding these basic principles we can target ares fr antiviral therapeutic potential.
A vaccine for hepatitis C virus (HCV) is not yet available. Immune responses that are able to protect against infection are possible, making the production of a vaccine a realistic goal. We have produced a unique HCV vaccine and are now poised to test our vaccine in novel humanised animal models. Our research will allow us to determine the immune responses responsible for providing protection against HCV. Our data will be highly significant for future HCV vaccine studies in humans.
Architecture Of The Hendra Virus Nucleocapsid And Implications For Replication
Funder
National Health and Medical Research Council
Funding Amount
$342,108.00
Summary
Hendra virus causes sporadic fatal outbreaks in horses, which may result in human deaths through direct contact with infected animals. The unanticipated surge of Hendra cases since mid-2011, the broad host range of the virus and the discovery of other related viruses worldwide highlight the epidemic potential of hendra-related paramyxoviruses. To improve our preparedness against paramyxoviruses, this Project aims at determining the structure of the viral replication machinery.
EEF1A1 Is Critical For HIV-1 Reverse Transcription And Replication
Funder
National Health and Medical Research Council
Funding Amount
$521,429.00
Summary
The project will investigate interaction between the AIDS virus, HIV-1, and the human cell it grows in specifically focusing on a human protein called eEF1A. Our research shows eEF1A is required for HIV-1 growth by regulating a step in the virus life cycle called reverse transcription. The goal of this project is investigate how interaction with eEF1A helps HIV-1 reverse transcription and to find drugs that block HIV-1 interaction with eEF1A.
This proposal investigates processes that regulate the cell cytoskeleton to control shape and the dynamics membranes, with a view to developing a generic antiviral therapy. As viruses rely upon the cell cytoskeleton to initiate an infection, we posit that enzymes that control the cytoskeleton can be targeted to block infection.
Characterize The Post-entry Events Of HIV Infection
Funder
National Health and Medical Research Council
Funding Amount
$605,190.00
Summary
For HIV to successful infect a target cell, it must properly remove the outer layers of its protective gears (outer viral protein coats) to allow the viral genetic materials to be replicate (duplicate and multiplied) for the generation of their ‘offspring viruses’. This process is known as viral uncoating, and it is arguably one of the least understood areas of HIV. In this proposal, we will use a number of complementary state-of-the-arts research tools to characterize the HIV uncoating process.
Identification Of Host Factors That Restrict Influenza Virus Replication In Macrophages
Funder
National Health and Medical Research Council
Funding Amount
$566,446.00
Summary
Influenza virus infects different cells in the airways, including immune cells (macrophages) and non-immune cells (epithelial cells). Epithelial cell infection results in virus amplification and release whereas macrophage infection leads to virus destruction. This project will identify cellular factors expressed by macrophages that block virus amplification and release. Identification of novel antiviral factors is an important step towards developing strategies to reduce influenza disease.
Targeting Myeloid Cells To Restrict Gamma-herpesvirus Spread
Funder
National Health and Medical Research Council
Funding Amount
$643,152.00
Summary
Gamma-herpesviruses infect most people and cause cancers. Vaccines to date have worked poorly. We have identified a key role for myeloid cells in infection that suggests a new approach. Interferons restrict infection in some myeloid cells. We will test whether inducing interferons can make all myeloid cells restrictive and reduce chronic infection. We will test then whether myeloid-restricting antibodies can recruit the same defences to provide a basis for vaccination.
Roles And Regulation Of Sphingosine Kinase 1 During Dengue Virus Infection
Funder
National Health and Medical Research Council
Funding Amount
$482,795.00
Summary
Dengue virus (DENV) infection is a global human disease with an estimated 50 million infections annually and there is no vaccine or therapy. DENV disease is worsended by the way the body responds to infection and we have investigated these responses. We know the virus changes a molecule in the body called sphingosine-kinase 1 (SK1), which normally controls if cell live or die and how they function. This study will characterise how DENV influences SK1 and if we can target this interaction to deve ....Dengue virus (DENV) infection is a global human disease with an estimated 50 million infections annually and there is no vaccine or therapy. DENV disease is worsended by the way the body responds to infection and we have investigated these responses. We know the virus changes a molecule in the body called sphingosine-kinase 1 (SK1), which normally controls if cell live or die and how they function. This study will characterise how DENV influences SK1 and if we can target this interaction to develop new drugs against DENV infection.Read moreRead less
Enhanced Expression Of The Epstein-Barr Virus Nuclear Antigen, EBNA1, As A Target For T-cell-Based Immunotherapy For Prevention Of Viral-Associated Diseases.
Funder
National Health and Medical Research Council
Funding Amount
$356,513.00
Summary
Epstein-Barr virus, (EBV) is a human herpesvirus associated with a range of human cancers. EBNA1, an important EBV antigen, was thought to be “immunologically silent” however, recent studies from our laboratory show that EBNA1 is recognized by our body's defence system and these observations raise the possibility that EBNA1 may be an exploitable, immuno-therapy target for treating EBV-associated cancers.