Dr Allison Abendroth
BSc (Honours First Class) PhD (Adelaide)

Sesqui Lecturer in Immunology

Head, Varicella Zoster Research Group

Address:
Room 601 Blackburn Building D06
University of Sydney NSW 2006

Phone:   +61  2  9351 6867

Mobile Phone:   +61  425 326 060
Fax:   +61  2  9351 4731
Email:   allisona@med.usyd.edu.au

Research Interests
Varicella Zoster Virus Immunology and Pathogenesis

Senior Scientist - Studying Varicella Zoster Virus Immunology and Pathogenesis. Supervisor of several Honour's and PhD Students. Supervisor of several Honour's & Phd Students at University of Sydney, Dept Infectious Diseases.

Dr Abendroth's research career started with a BSc Hons (first class) and PhD performed at the University of Adelaide on the immunobiology of Herpes Simplex Virus. Post-doctoral studies at Stanford University enabled her to further her career interests in herpes virus immunobiology and pathogenesis.

On returning to Australia she was awarded a Rolf Edgar Lake Fellowship from the University of Sydney and set up the VZV Research Group at the Westmead Millennium Institute. In February 2004 Dr Abendroth was appointed as a Sesqui lecturer in Immunology and is the third year Immunology Course Coordinator. Her lab focuses on many aspects of VZV immunobiology and pathogenesis and consists of Honours and PhD students and research personnel. The research programme is currently being established in the Department of Immunology and Infectious Diseases on level six of the Blackburn Building.

Research Interests

Varicella zoster virus (VZV is a herpesvirus which infects up to 90% of the population.  VZV causes chickenpox (varicella) predominantly in childhood and shingles (herpes zoster) in middle to old age people.  Whilst VZV usually causes relatively mild disease in healthy individuals, VZV still causes significant morbidity in children and adults.  VZV causes life-threatening disease in immunocompromised individuals such as patients who are elderly or have HIV disease.  Herpes zoster affects many elderly individuals and a major complication is prolonged severe pain or post-herpetic neuralgia (PHN), both severely debilitating and which often require follow-up medical care for months or years after the initial attack.  Despite its significant impact on the community, little is known about the molecular details of how this virus functions.

Dr Abendroth's team aims to improve our understanding of how VZV infection affects specialised human cells in order to make further advances in antiviral therapies as well as improve vaccine design for the treatment or prevention of VZV disease and the crippling complication of PHN.

Current studies include:

1. Determining how VZV actively avoids detection by the immune system. We aim to identify the mechanism and viral genes responsible for interfering with the expression of molecules which are essential for our immune system
2. Assessing whether VZV infection of specialised immune cells (called dendritic cells) will affect their ability to function and interact with other immune cells (called T cells)
3. Assessing how VZV interacts in human nerve cells (neurons) and whether infected neurons undergo specially programmed cell death (apoptosis), and
4. Characterising the immunohistology of human sensory ganglia during herpes zoster (shingles)
5. Examining how different human cells change when they are infected with VZV. A new and exciting technology called DNA microarray now makes it possible to examine the expression of many thousands of genes in one experiment

Recent Publications

Hood, Cummingham, Slobedman, Boadle and Abendroth (2003). Varicella zoster virus infected human sensory neurons are resistant to apoptosis yet human foreskin fibroblasts are susceptible: evidence for cell-type specific apoptosis induced by VZV infection. Journal of Virology, 77: 12852-64.

Morrow, Slobedman, Cunningham & Abendroth (2003). Varicella zoster virus productively infects mature dendritic cells and alters their immune function. Journal of Virology, 77: 4950-4959.

Abendroth, Morrow, Cunningham & Slobedman (2001). Varicella zoster virus infection of human dendritic cells and transmission to T cells: Implications for virus dissemination in the host. Journal of Virology; 75: 6183-6192.

Abendroth, Lin, Slobedman, Ploegh & Arvin (2001). Varicella Zoster Virus Retains Major Histocompatibility Complex Class I Antigens in the Golgi of Infected Cells. Journal of Virology; 75: 4878-4888.

Abendroth & Arvin (2001). Immune evasion as a pathogenic mechanism of varicella zoster virus. Seminars in Immunology; 13: 27-39.

Abendroth, Slobedman, Lee, Wallace & Arvin (2000). Modulation of major histocompatibility class II expression by varicella zoster virus. Journal of Virology; 74: 1900-1907.