Professor Martin J Allday

Viral persistence and human cancer

A significant subset of viruses produce what is known as persistent infections. This means that after primary infection the host carries the virus for life, generally with no obvious symptoms and in a state of equilibrium with the immune system.
Such long-term, intimate relationships between virus and host can – on rare occasions (often associated with impairment of the immune system) – result in cancer. For example in humans Epstein-Barr virus (EBV) is associated with several B cell lymphomas and carcinomas, Hepatitis B and C viruses are linked to hepatocellular carcinoma and Karposi’s Sarcoma (KS)-associated virus (KSHV) is involved in the pathogenesis of KS and two B cell lymphomas.
We are interested in the circumstances that lead to the development of virus-associated cancers and specifically the contribution EBV makes to the pathogenesis of various B cell lymphomas. We are trying to understand how this relates to normal persistence of the virus in a latent form and whether the virus can provide specific targets for therapeutic intervention.

Specific Research Themes:

How does Epstein-Barr virus (EBV) disrupt checkpoints that normally regulate cell growth and division? 

How does EBV enhance the survival of B cells under conditions that would normally result in programmed cell death (apoptosis)?

What roles do a family of EBV nuclear proteins (EBNAs 3A, 3B and 3C) play in re-programming B cells to make them and their progeny more likely to become cancerous?

Link here to my Research Page:

Selected publications:

Anderton, E. Yee, J. Smith, P. Crook, T. White, R.E. and Allday, M.J. (2007) Two Epstein-Barr virus (EBV) oncoproteins cooperate to repress expression of the pro-apoptotic tumour-suppressor Bim: clues to the pathogenesis of Burkitt’s lymphoma. Oncogene – ePubMed ahead of print.
Leao, M.E. Anderton, E. Wade, M. Meekings, K. and Allday, M.J. (2007) Epstein-Barr virus (EBV)-induced resistance to drugs that activate the mitotic spindle assembly checkpoint in Burkitt’s lymphoma cells. J. Virol. 81, 248-60.
O’Nions, J. Turner, A. Craig, R. and Allday, M.J. (2006) Epstein-Barr virus selectively deregulates the DNA-damage responses of normal B cells, but has no detectable effect on the tumour suppressor p53. J. Virol. 80, 12408-13.
Spyer, M. and Allday, M.J. (2006) C-terminal binding protein (CtBP) associates with centrosomes throughout mitosis. Cell Cycle 5, 530-537.
Brown, A.C. Baigent, SJ. Smith, L.P. Chatoo, J. Petherbridge, L.J. Monaghan, P. Allday, M.J. and Nair, V. (2006) Interaction of Meq and CtBP is critical for tumour induction of lymphomas by Marek’s disease virus. Proc. Natl. Acad. Sci. USA 103, 1687-92.
O’Nions, J. and Allday, M.J. (2004) Deregulation of the cell cycle by Epstein-Barr virus. Advances in Cancer Research 92, 119-178.
O’Nions, J. and Allday, M.J. (2003) Epstein-Barr virus can inhibit genotoxin-induced G1 arrest downstream of p53 by preventing the inactivation of CDK2. Oncogene 22, 7181-7191.