The Australian Research Data Commons (ARDC) invites you to participate in a short survey about your
interaction with the ARDC and use of our national research infrastructure and services. The survey will take
approximately 5 minutes and is anonymous. It’s open to anyone who uses our digital research infrastructure
services including Reasearch Link Australia.
We will use the information you provide to improve the national research infrastructure and services we
deliver and to report on user satisfaction to the Australian Government’s National Collaborative Research
Infrastructure Strategy (NCRIS) program.
Please take a few minutes to provide your input. The survey closes COB Friday 29 May 2026.
Complete the 5 min survey now by clicking on the link below.
Elucidating The Activation Mechanism Of The HIV-1 Envelope Glycoproteins, Gp120-gp41
Funder
National Health and Medical Research Council
Funding Amount
$636,973.00
Summary
Antiretrovirals prolong the life of HIV+ people, however toxicity and resistance issues persist. We aim to understand how the HIV surface proteins effect viral entry in order to identify new antiviral targets.
Delineation Of Receptor-activated Conformational Signalling Pathways In HIV-1 Envelope Glycoproteins
Funder
National Health and Medical Research Council
Funding Amount
$834,478.00
Summary
Although antiretroviral therapy has prolonged the life of people infected with HIV, the virus rapidly develops resistance. Therefore it is essential to develop new antiviral agents to combat HIV infection. The first stages of infection include the process of the virus attaching to cellular receptors and the fusion of viral and cellular membranes leading to entry. In this project we seek to understand how the surface proteins of the virus mediate viral entry and identify new antiviral targets.
Influenza remains an important disease and exacts a high toll in both morbidity and mortality each year. This project will identify the carbohydrates that are utilised by influenza virus to initiate infection throughout the body and map how these carbohydrates interact with the key viral surface proteins. This research will provide new insight into the emergence of new influenza virus strains and cross-species pathogenicity.
Structure And Function Of The Hepatitis C Virus Glycoproteins E1 And E2.
Funder
National Health and Medical Research Council
Funding Amount
$533,828.00
Summary
Hepatitis C virus (HCV) infects approximately 3 % of the global human population with 150,000-200,000 HCV-infected individuals currently living in Australia. Chronic HCV infection is associated with recurrent, progressively worsening liver disease, liver cirrhosis and hepatocellular carcinoma. The current therapy (interferon-ribavirin) is effective in only 40 % of patients and is often associated with severe side-effects. The mechanisms that HCV uses to replicate in liver cells is poorly underst ....Hepatitis C virus (HCV) infects approximately 3 % of the global human population with 150,000-200,000 HCV-infected individuals currently living in Australia. Chronic HCV infection is associated with recurrent, progressively worsening liver disease, liver cirrhosis and hepatocellular carcinoma. The current therapy (interferon-ribavirin) is effective in only 40 % of patients and is often associated with severe side-effects. The mechanisms that HCV uses to replicate in liver cells is poorly understood. In this project we aim to better understand how the viral glycoproteins, E1 and E2, function in the initiation of infection. In particular, we will examine how these glycoproteins bind to liver cell receptors and then mediate virus-cell membrane fusion. These processes lead to the penetration of the HCV genetic material into the cell where it is replicated. These studies are essential for the discovery of new targets for antiviral agents and vaccines.Read moreRead less
Hepatitis C Virus infects 3% of the world's population causing recurring liver disease, cirrhosis and hepatocellular carcinoma. To infect a liver cell, the viral glycoproteins attach to cell surface molecules wher they are activated to mediate merger of the viral and cellular membranes. This project grant will explore how the viral glycopropteins become activated and obtain essential structural information on the viral glycoproteins. These studies will help us to design antiviral agents.
Structural And Functional Role Of HIV-1 Gp41 Terminal Interactions In The Membrane Fusion Mechanism
Funder
National Health and Medical Research Council
Funding Amount
$529,632.00
Summary
Approximately 40 million individuals are currently living with HIV. The viral glycoproteins, gp120-gp41, mediate the first stage of infection, membrane fusion, and thus serve as targets for vaccines and antiviral agents. Thi proposal seeks to assess the structure and function of a potential new drug target in gp120-gp41. These studies may lead to the identification of a new antiviral that blocks membrane fusion. Such agents can be added to antiviral drug cocktails for more effective therapy.
Hepatitis C virus (HCV), the main cause of of post-transfusion and community -acquired non-A, non-B hepatitis, infects approximately 170 million humans world-wide with some 135,000 infections in Australia alone. HCV is hyper-endemic in intravenous blood users with typical prevalence rates of 60-70%. About 75-80% of infected individuals develop a chronic infection, usually resulting in recurrent, progressively worsening liver damage. Cirrhosis develops in 10-20% of chronic cases while 1-5% of chr ....Hepatitis C virus (HCV), the main cause of of post-transfusion and community -acquired non-A, non-B hepatitis, infects approximately 170 million humans world-wide with some 135,000 infections in Australia alone. HCV is hyper-endemic in intravenous blood users with typical prevalence rates of 60-70%. About 75-80% of infected individuals develop a chronic infection, usually resulting in recurrent, progressively worsening liver damage. Cirrhosis develops in 10-20% of chronic cases while 1-5% of chronic carriers develop liver cancer. Development of an effective vaccine is complicated due to the highly variable nature of the virus. Approved therapies include alpha-interferon and alpha interferon-ribavirin combinations but these treatments induce efficacious responses in only 20-30% of patients and often have severe side-effects. It is assumed that after attachment of HCV to the cell surface, the virus is internalised by the cell and undergoes fusion with a cellular compartment referred to as an endosome. The low pH environment of the endosome is presumed to trigger viral fusion via its cell surface glycoproteins and empties the replication machinery of the virus into the cell. No reliable systems for the propagation of HCV are available thereby limiting studies into the mechanisms of how HCV infects cells and the development of vaccines. Recently a cell surface molecule, CD81, was identified as a possible receptor for the attachment of HCV to susceptible cells. Our aim is to 1) develop model systems for studying HCV entry and fusion and 2) further characterise the interaction of the HCV glycoproteins with CD81 with the goal of obtaining a three-dimersional structure of the interaction . These studies will address the fundamental questions of how HCV enters cells leading new avenues for the design of inhibitors of HCV entry.Read moreRead less
Adaptive Changes In HIV-1 Subtype C Envelope Glycoproteins Contributing To Pathogenicity.
Funder
National Health and Medical Research Council
Funding Amount
$427,648.00
Summary
HIV exists as multiple subtypes. The most commonly studied is type B (B-HIV). B-HIV is common in North America, Europe and Asia, but accounts for only a small fraction of HIV infections worldwide. Type C HIV (C-HIV) in Africa and Asia accounts for the majority of infections worldwide, yet very little is known about how C-HIV causes AIDS. We aim to understand how C-HIV causes AIDS. This is critical for development of drugs and vaccines specifically designed for those who are most urgently need.