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.
Inhibition Of Cellcell Actin-based Motility During Poxvirus Infection By The Kinase Inhibitor Glivec
Funder
National Health and Medical Research Council
Funding Amount
$92,950.00
Summary
Although smallpox, one of the deadliest human pathogens, was eradicated in 1980, the current global climate has resulted in fears that smallpox may be used as a biological weapon. Unfortunately the smallpox vaccine poses a serious health hazard to certain people. We have shown that Glivec, a drug used to treat cancer, has potent anti-viral affects on poxvirus replication. This project will test the effectiveness of Glivec in treating smallpox in an animal model and study how it acts.
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.
The Role Of Chemokines In Establishing HIV Latency
Funder
National Health and Medical Research Council
Funding Amount
$372,049.00
Summary
Although antiviral therapy is effective in controlling HIV, therapy must be continued life-long because the virus cannot be cleared from long lived infected CD4+ T cells that are silently or latently infected. In this proposal we will explore the mechanism of how HIV can enter these resting CD4+ T-cells and establish long lived latent infection. Understanding this process may potentially lead to new strategies to cure HIV infection.