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Prof Clare Jolly
1st Floor
Cruciform Building
Gower Street
Prof Clare Jolly profile picture
  • Professor of Virology
  • Div of Infection & Immunity
  • Faculty of Medical Sciences
Research Themes
Research Summary

UNAIDS estimates around 33 million people are living with HIV/AIDS and approximately 25 million have died. While the ultimate goal remains the development of an effective HIV-1 vaccine, there is also a need for new and improved anti-viral strategies and this requires a better understanding of the molecular cell biology and pathogenesis of HIV-1 infection.

The research interests of my laboratory are broadly aimed at understanding how HIV-1 assembles in and disseminates between CD4 T cells - the main targets for HIV-1 infection in vivo. 

Cell-cell spread at Virological Synapses

Previous work by us and others have shown that direct cell-cell spread of HIV-1 between T cells is a very efficient mode of viral dissemination. Cell-cell spread of HIV-1 takes place across a virus-induced multimolecular structure called the virological synapse (VS)(see publications). Our identification of the HIV-1 T cell VS provided a molecular framework to explain how cell-cell spread of HIV-1 occurs and why it so efficient. The VS is characterised by cytoskeleton-driven recruitment of viral proteins, adhesion molecules and entry receptors (CD4 and chemokine receptors) to the site of contact between an HIV-1-infected T cell and a susceptible target T cell. This promotes rapid infection of the target cell by focussing virus assembly and budding to the site of cell-cell contact. Increasing evidence shows that cell-cell confers a number of replicative advantages to the virus, including more efficient spread and may allow HIV-1 to evade aspects of the humoral immune response, innate antiviral restriction factors and antiretroviral drugs. Thus cell-cell spread at VS may pose a considerable barrier to HIV-1 eradication from the host. The VS shares many similarities with a well-described structure called the immunological synapse (IS) and we hypothesise that HIV-1 spread at the VS may involve related cellular machinery, and that HIV-1 hijacks elements of the regulated secretory pathway to transport viral proteins and coordinate assembly and egress. Our current research is focussed on delineating the contribution of T cell trafficking pathways and associated molecules to HIV-1 pathogenesis in T cells. We are also seeking to identify cellular proteins that regulate VS formation and to delineate how they contribute to HIV-1 replication and spread.

The cell biology of HIV-1 replication

Virus assembly is a complex series of well-orchestrated events, in which all components must be delivered to the appropriate cellular location in a temporally and spatially controlled way. We are interested in determining how the viral envelope glycoprotein (Env) and the major structural protein Gag are trafficked to sites of HIV-1 assembly in T cells during both cell-free and cell-cell spread. We are particularly interested in the trafficking of Env and its incorporation into virions because of the essential role Env plays in viral infectivity, tropism and VS formation.

Teaching Summary

I lecture on the Molecular Virology course and MSc programs. 

Academic Background
2000   Doctor of Philosophy University of Melbourne
1995   Bachelor of Science (Honours) University of Melbourne
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