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.
HIV infection of CD4+ lymphocytes leads to a high rate of reproduction of new virus. However, in the brain, HIV infection of the astrocytes does not yield high levels of new virus. HIV is genetically active in these astrocytes, producing high levels of the messenger molecules, the so-called mRNA, that code for the proteins required for a new virus particle. We have determined that these HIV mRNAs are specifically prevented from translating into protein. The mechanisms controlling protein transla ....HIV infection of CD4+ lymphocytes leads to a high rate of reproduction of new virus. However, in the brain, HIV infection of the astrocytes does not yield high levels of new virus. HIV is genetically active in these astrocytes, producing high levels of the messenger molecules, the so-called mRNA, that code for the proteins required for a new virus particle. We have determined that these HIV mRNAs are specifically prevented from translating into protein. The mechanisms controlling protein translation from RNA are relatively poorly understood compared with the other control points of cellular gene expression, such as the synthesis of mRNA. This project examines how astrocytes rapidly detect the presence of HIV mRNA and alter their translation machinery to halt the expression of HIV protein. This host defence mechanism involves two key components; the cellular component that identifies and responds to the viral mRNA, and the structural features of the HIV mRNA that enable the cell to detect its viral origin. We will study how translation of HIV proteins requires both HIV and cellular factors. We will determine the impact of both viral RNA elements and viral RNA binding proteins on the translation of viral and cellular proteins. The contribution of the type-1 interferons that are produced in response to viral infection will be studied for their role in augmenting the inhibition of HIV protein translation. Since HIV infected astrocytes significantly contribute to the onset of AIDS dementia, we will sees a strategy to lock HIV into a dormant state in the brain and thereby prevent the neurodegenerative disease associated with HIV. We will use the anti-viral mechanism blocking HIV protein translation in astrocytes to protect other cell populations, such as the CD4+ lymphocytes, from HIV infection. These studies will also give insights into the general mechanisms for translational control of gene expression in human cells.Read moreRead less
Tuberculosis kills more people than any other infectious disease, and approximately one-third of the world's population is latently infected with Mycobacterium tuberculosis. This situation is largely due to the low efficacy of the only licensed TB vaccine, BCG, and the 'black box' of what constitutes protection against TB. This project aims to unravel the mechanisms of protective immunity against TB to develop a highly protective vaccine.
HIV is a rapidly evolving virus, and within an infected individual it continually acquires new mutations and joins together mutations by recombination. We have developed a novel system for studying recombination, and find that different individuals have different recombination rates, which may contribute to why some individuals survive longer. This project aims to identify the mechanisms responsible for differing recombination rates and how we can alter these to improve patient outcome.
The Future Of HIV Care - Long Term Remission And Eliminating Co-morbidities
Funder
National Health and Medical Research Council
Funding Amount
$577,189.00
Summary
Despite the great successes in antiretroviral therapy (ART) in reducing HIV-associated mortality, treatment is life long and there is no cure. The major barrier to a cure for HIV is the persistence of long lived latently infected cells on ART. Over the next five years I will discover, develop, optimise and evaluate novel interventions to eliminate latently infected cells, long lived infected cells in the liver and enhance HIV-specific immunity through immunotherapy.
Understanding And Preventing Chronic Disease In People Living With HIV
Funder
National Health and Medical Research Council
Funding Amount
$367,946.00
Summary
Australia’s ageing population is increasingly at risk of chronic diseases such as heart disease and diabetes. For Australians who are living with HIV, these diseases occur more frequently and at an earlier age. I will be investigating the underlying reasons for this increase in risk and will test innovative online systems that help people living with HIV reduce their risk of chronic disease. This work will provide important information for Australians at risk of developing chronic disease.
Prevention Of HIV-1 Infection By Adeno Associated Virus Vector-delivered Broadly Neutralizing Antibodies Or Antibody-like Molecules
Funder
National Health and Medical Research Council
Funding Amount
$875,854.00
Summary
A promising neutralizing molecule has boosted hopes of an HIV vaccine. It remains unknown how well this molecule prevents HIV infection under conditions reflecting “real world” exposure, including exposure to HIV in the form of cells carrying virus or free-floating virus in the presence of semen. We will assess this molecule for their ability to inhibit transmission of HIV-like viruses under these conditions. These experiments will define requirements to protect against HIV infection.
The Human Immunodeficiency Virus (HIV) is a virus that infects and kills the cells of your immune system. This infection eventually leads to the Acquired Immune Deficiency Syndrome (AIDS). An important aspect in preventing infection is to study how HIV enters immune cells and how infection spreads. Our lab is researching drugs to block the entry of HIV in immune cells, which can hopefully be used together with existing anti-HIV drugs to slow down the spread of the virus and the onset of AIDS.
A Novel RNA Repressor Element Regulates HIV-1 Replication
Funder
National Health and Medical Research Council
Funding Amount
$341,453.00
Summary
HIV-1 causes acquired immunodeficiency syndrome, with up to 40 million infected people and 5 million infected annually. The spatio-temporal regulation of HIV-1 reverse transcription has recently been recognised as a possible new drug target. Our research has revealed a novel repressor of reverse transcripiton (RRT). The RRT plays a major role in regulating the spatio-temporal regulation of reverse transcripiton. Targetting the RRT function would be a novel means to combat HIV-1 infection.
Addressing The Major Challenges In HIV Vaccine And Cure Research
Funder
National Health and Medical Research Council
Funding Amount
$16,136,755.00
Summary
HIV remains one of the defining global health challenge of our times. 37 million people are living with HIV with 2 million new infections each year. Despite advances in management of HIV infection with antiretroviral therapy, there is still no cure, no effective vaccine, and several co-infections reduce life expectancy. This program assembles Australia’s leading HIV researchers to use innovative basic and translational science to tackle priority areas in controlling the HIV epidemic.