Functional Roles Of The Tegument Proteins Of Herpes Simplex Virus Type 1
Funder
National Health and Medical Research Council
Funding Amount
$461,597.00
Summary
The occurrence of herpes simplex virus (HSV) in the general population is very high (up to 60%). HSV enters the human body via the skin before entering nerve cells where it lies dormant in most people. Intermittently the virus reactivates and usually forms blisters at the skin when it sheds. The aim of this project is to define a molecular interaction network at the protein level during the course of infection of a host cell. This information will provide new targets for design of antivirals.
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.
The Role Of Varicella Zoster Virus In Modulating Cutaneous Infection
Funder
National Health and Medical Research Council
Funding Amount
$555,892.00
Summary
Varicella zoster virus (VZV) causes two skin diseases: chickenpox and shingles. VZV can causes significant morbidity in children and adults and life-threatening disease in immunocompromised people. This project aims to improve our understanding of how VZV affects the function of specialised skin cells to provide information for the development of a better vaccine to lessen the impact of VZV disease on the community.
Defining Key Mechanisms That Underpin Neuropathogenesis Of Varicella Zoster Virus During Herpes Zoster
Funder
National Health and Medical Research Council
Funding Amount
$616,518.00
Summary
Varicella zoster virus (VZV) is a herpesvirus which causes chicken pox and shingles. Shingles affects many elderly people and a major complication is prolonged severe neuropathic pain, often needing follow-up medical care for months to years. Despite its impact on the community, little is known about how this virus functions and causes disease. We aim to improve our understanding of how VZV interacts with nerve cells to provide essential new information for the development of effective treatment ....Varicella zoster virus (VZV) is a herpesvirus which causes chicken pox and shingles. Shingles affects many elderly people and a major complication is prolonged severe neuropathic pain, often needing follow-up medical care for months to years. Despite its impact on the community, little is known about how this virus functions and causes disease. We aim to improve our understanding of how VZV interacts with nerve cells to provide essential new information for the development of effective treatments for shingles and associated neuropathic pain.Read moreRead less
Current vaccines rely on immune components in the blood. We are taking a different approach, which focuses on immunity at the body surfaces. These are the areas where pathogens first gain access to the body and we have shown that immune cells in these regions are far more potent than those that need to be recruited from the circulation.
Herpesviruses infect us all and cause cancer, blindness, and congenital disability. Developing vaccines requires information from both patients and experimental animals. CD4 T cells seem to suppress directly virus replication, and cells in the nose provide an important way for herpesviruses to get in. We will test whether CD4 T cells can clear nasal infection; what targets they recognize; and how they act. Thus we can establish whether CD4 T cell-directed vaccines might protect against disease.
Mechanisms By Which Varicella Zoster Virus And Herpes Simplex Virus Control Host Functions To Enhance Pathogenesis
Funder
National Health and Medical Research Council
Funding Amount
$631,999.00
Summary
Varicella Zoster Virus and Herpes Simplex Virus are alpha-herpesviruses that cause diseases in a majority of the human population. This proposal will explore issues fundamental to disease and pathogenesis of these two closely related herpesviruses, focusing on how these viruses can control host function. In particular, we will define the interactions between these viruses and the natural killer (NK) cell response.
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 A Novel Mechanism Of Control Of Host Functions By Human Cytomegalovirus That Enhances Viral Pathogenesis
Funder
National Health and Medical Research Council
Funding Amount
$616,518.00
Summary
Human cytomegalovirus (HCMV) remains a significant human pathogen which causes serious and often life-threatening disease in immunosuppressed people such as bone marrow and solid organ transplant patients and in unborn babies infected during pregnancy. This project will define how HCMV controls host defences by actively modifying the cells it infects to create an environment favourable to continued viral infection and disease.
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.