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Understanding The Role Of Ongoing Viral Activity In Herpes Simplex Virus Latency
Funder
National Health and Medical Research Council
Funding Amount
$980,762.00
Summary
The virus that causes cold sores and genital herpes has a dormant phase from which renewed infection can recur. We recently discovered that this dormant phase is more active than we thought and we now want to learn how the body acts to suppress the virus so that these defence mechanisms might be improved to stop recurrent infections.
Targeting MiRNA Biogenesis To Treat Herpes Simplex Virus Latency
Funder
National Health and Medical Research Council
Funding Amount
$800,085.00
Summary
Herpes simplex virus (HSV) causes cold sores in most infected people, but can also cause blindness and fatal brain infections. The biggest problem with HSV is that it never completely goes away - the virus hides in a part of the nervous system and can come out to cause disease over and over again. We have recently discovered a gene in people that the virus needs to maintain itself in this hidden state. In this project we will use this exciting discovery to work towards a cure for HSV.
A Humanised Mouse Model For Herpes Simplex Virus Pathogenesis
Funder
National Health and Medical Research Council
Funding Amount
$277,109.00
Summary
Herpes simplex virus (HSV) causes cold sores and genital herpes, diseases that persist and recur. This persistence is because HSV has several ways of stopping the body from detecting and eliminating the cells that it infects. This project will generate new tools that will help us to understand one of the ways that HSV hides from our defences and may be useful in developing immune-based therapies to treat the infection.
Defining The Mechanism Of Assembly Of Herpes Simplex Virus In The Neuronal Growth Cone And Its Subsequent Exit To Epithelial Cells
Funder
National Health and Medical Research Council
Funding Amount
$774,624.00
Summary
Herpes simplex virus (HSV) causes dormant infection of nerve cell bodies near the spine. It periodically reactivates to be transported along nerves to the skin where it causes oral, genital or neonatal herpes and mediates HIV superinfection. HSV assembles into its final form in the terminal part of the axon just prior to crossing into skin. Elucidating the mechanism of HSV assembly and exit will facilitate new strategies for antiviral agents and immune treatment for HSV and similar viruses.
A Proteome-wide Approach To Anti-viral Immunity And Vaccine Development
Funder
National Health and Medical Research Council
Funding Amount
$622,655.00
Summary
We know that many parts of viruses are displayed to the immune system, but at present the exact fragments are difficult to predict, we do not know all the genes in our bodies that control this process and we also need better methods to study the way some viruses (e.g. the cold sore virus) avoid detection. This project will study these problems with the overall goal of improving vaccine design, understanding immune deficiency and how viruses fight back against our immune system.
The Role Of A Novel Cytokine Of The Innate Immune Response In Viral Infection
Funder
National Health and Medical Research Council
Funding Amount
$344,407.00
Summary
Sexually transmitted infections represent a critical global health and socioeconomic problem with over 1 billion new cases per annum. I propose a world-first description of a new protein that has a protective role against herpes simplex virus (HSV) infection of female reproductive tract. This unique protein, called interferon epsilon, was discovered in our laboratory. This project will facilitate development of new therapeutic approaches of benefit in HSV-2 infection.
The Mechanism Of HSV-1 Transport In Sensory Axons And Its Unique Assembly At The Axon Terminus
Funder
National Health and Medical Research Council
Funding Amount
$670,284.00
Summary
Herpes simplex viruses 1 and 2 cause common diseases such as genital herpes and, occasionally, neonatal deaths and encephalitis and predisposes to HIV infection. New antiviral strategies are required for resistant viruses for control. These aims will be facilitated by understanding how HSV is transported down nerves and across into skin. In this study, we will define how a key viral protein plays a major role in assembly of the virus at the tip of the nerve before it enters skin.
Anti-viral Immunity And The Survival Of Cells Infected With Herpes Simplex Virus In Vivo
Funder
National Health and Medical Research Council
Funding Amount
$574,890.00
Summary
Herpes simplex virus causes cold sores and genital herpes. A person can only catch the virus once in their life, but it stays in their body and can cause occasional outbreaks of disease. This recurrent disease can be frequent and severe. The place where the herpes virus hides in a dormant state between outbreaks is in the nervous system. This project aims to learn more about how the virus becomes dormant and also whether the immune system is important in keeping the virus in this state.
Defining The Contribution Of Skin Gamma Delta T Cells To Cutaneous Immunosurveillance, Immunity And Disease After HSV Infection.
Funder
National Health and Medical Research Council
Funding Amount
$601,386.00
Summary
Herpes simplex virus (HSV) causes genital herpes and encephalitis. Disease is severe in the immunocompromised and the newborn. HSV enters through breaks in the skin or mucosa, where it first encounters gamma delta T cells. We have recently made the key finding that HSV can infect gamma delta T-cells shortly after inoculation. Here we will study how they contribute to the immune response when a virus enters the skin in mice and human tissues. This may lead development of new topical antiviral vac ....Herpes simplex virus (HSV) causes genital herpes and encephalitis. Disease is severe in the immunocompromised and the newborn. HSV enters through breaks in the skin or mucosa, where it first encounters gamma delta T cells. We have recently made the key finding that HSV can infect gamma delta T-cells shortly after inoculation. Here we will study how they contribute to the immune response when a virus enters the skin in mice and human tissues. This may lead development of new topical antiviral vaccines.Read moreRead less
Structural Basis Of Substrate Recognition By The Membrane-Associated E3 Ubiquitin Ligases
Funder
National Health and Medical Research Council
Funding Amount
$415,244.00
Summary
Membrane-associated E3 ubiquitin ligases control cellular levels of important immunoregulatory molecules and occur in both host- and virus-encoded forms. Target selectivity maps to the transmembrane domains of ligases and their substrates in a little-studied mode of intramembrane molecular recognition. Our goal is to determine the physical basis of this interaction by establishing which sequences drive the association and providing atomic-resolution structures of the membrane-embedded complexes.