The Impact Of HIV Integration Sites On Eliminating HIV Latency
Funder
National Health and Medical Research Council
Funding Amount
$778,313.00
Summary
Current antiviral therapy for HIV controls virus production and allows recovery but does not eliminate the silent infection that prevents complete virus elimination and cure. We will examine two ways that HIV can silently infect T cells for differences in the sites at which the HIV DNA inserts into the genome. We will examine the way in which these differences at the genomic level may limit the ability to activate and eliminate persistent infection in memory T cells.
The Role Of Chemokine Signalling In Maintenance Of The Latent HIV Reservoir
Funder
National Health and Medical Research Council
Funding Amount
$92,161.00
Summary
HIV cure research aims to eliminate cells with HIV in their DNA. These cells have higher levels of a receptor, CCR6, signalling through which causes migration to and concentration in the gut. This gut migration may help to maintain the HIV reservoir by bringing susceptible cells close to infected cells. We will assess the effect of blocking CCR6 signalling on the ability to infect these cells with HIV in the laboratory and its effect on the reservoir of an analogous virus in macaques.
HIV Phenotypes Important For The Establishment Of Persistent Reservoirs In The Central Nervous System And Which Impact Neurotropism And Neuropathogenesis
Funder
National Health and Medical Research Council
Funding Amount
$762,492.00
Summary
This grant will determine whether or not the CNS is a reservoir for HIV and identify the cellular targets of persistent infection and type of HIV-1 present.
The primary aim of this grants to determine how HIV spreads through our immune system. The above knowledge will determine key Achille’s Heel moments in the HIV life cycle and thus lead to better therapeutic HIV treatments/prevention.
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.
HIV infection is a dynamic process, in which the host immune response tries to control viral growth and keep up with the rapid evolution of the virus. This project assembles an interdisciplinary team of mathematicians and biologists to use a modelling approach to understand the dynamics of viral infection, viral evolution, and immune control in the infected individual. The insights gained from this project will help in the development of new drug and vaccination strategies.
Characterising The Genotypic And Phenotypic Properties Of The HIV-1 Viral Reservoir
Funder
National Health and Medical Research Council
Funding Amount
$316,819.00
Summary
Current drug treatments can not eradicate HIV from the body. This is because HIV can infect and establish a latent or “silent” infection in long-lived cells of the immune system that can re-emerge out of these cells when drug treatment is stopped. This project aims to find out how these cells become infected and what type of HIV is infecting them. The results from this study will help us better understand the latent infection and will help researchers design ways to eradicate HIV.
Envelope Glycoprotein Determinants Of HIV-1 Subtype C Tropism And Pathogenicity
Funder
National Health and Medical Research Council
Funding Amount
$657,745.00
Summary
HIV-1 subtype C is the most common subtype of HIV-w worldwide, yet we know comparatively little about how it causes disease in humans. This study will elucidate how HIV-1 subtype C evolves in patients to become more pathogenic over time.
A New Monocyte Atherogenic Phenotype In Chronic HIV Disease.
Funder
National Health and Medical Research Council
Funding Amount
$632,037.00
Summary
Most HIV+ people in Australia now die from cardiovascular disease, caused by atherosclerosis or thickening of coronary arteries. The ability of a white blood cell called the monocyte to prevent atherosclerosis is impaired in HIV. This project aims to understand how HIV does this and how we can reverse the effect. Understanding these processes will also help improve treatments to reduce heart disease in people with other chronic inflammatory conditions.
Viruses are considered neither live nor dead, and it is understood that biological process within a virus must occur after it infects a cell. Our work reveals a previous unknown step in HIV known as pre-entry priming. These discoveries challenge our current dogma of how viruses function, and imply this pre-entry priming process is a built in mechanism for HIV to protect itself. This proposal will redefine our understanding of HIV and explore novel HIV vaccine design through these discoveries.