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Finding novel ways to treat cancers caused by viruses

   Faculty of Biological Sciences

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  Dr A MacDonald  Applications accepted all year round  Self-Funded PhD Students Only

About the Project

Viruses are associated with up to 15% of cancers worldwide, representing approximately 1.2 million cancer cases worldwide annually. We are primarily interested in studying the molecular biology of 2 of the 7 viruses that have been identified as human tumour viruses, Human Papillomavirus and Merkel cell polyomavirus.

The Macdonald laboratory utilises a range of cutting-edge approaches to globally identify how viral proteins affect the cellular environment. This is helping to identify essential virus-host cell interactions which we can target by novel antiviral strategies to inhibit virus replication and transformation. 

You will be involved in a highly novel project which utilises a multidisiplinary approach and cutting-edge methodology including quantitative proteomics, imaging, cell biology and structural-based rational drug design approaches to produce target compounds which may form the basis of future antiviral reagents.

The PhD will provide a wide range of molecular biology, cell culture and virological techniques.

More information on the Whitehouse lab can be found at : www.fbs.leeds.ac.uk/staff/Macdonald_A/

Informal enquiries please contact [Email Address Removed]

Funding Notes

Self-funded students: International or domestic self-funded or scholarship/fellowship PhD students are always welcome to apply. International students must have a good command of both written and spoken English. Most importantly, bench fees will be required if you are self-funded. Applications can be made throughout the year.


Selected Macdonald group publications
37. Whitehouse & Macdonald (2015). Stathmin drives virus-induced metastasis. Oncotarget. In press.
36. Richards, Wasson, Watherston, Doble, Blair, Wittmann & Macdonald (2015). Human papillomavirus (HPV) E7 protein antagonises a novel imiquimod-induced inflammatory pathway in primary keratinocytes. Scientific Reports. 13;5: 12922.
35. Muller, Wasson, Bhatia, Boxall, Millan, Goh, Haas, Stonehouse & Macdonald (2015). YIP1 family member 4 (YIPF4) is a novel cellular binding partner of the papillomavirus E5 proteins. Scientific Reports. 3;5:12523.
34. Igloi, Kazlauskas, Saksela, Macdonald, Mankouri and Harris (2015). The hepatitis C virus NS5A protein blocks EGFR degradation via a proline motif dependent interaction. Journal of General Virology pii: vir.0.000145. doi: 10.1099/vir.0.000145.
33. Barnard, Long, Martin, Miles, Edwards, Tomlinson, Macdonald & Wilson*. (2015). Selective and Potent Proteomimetic Inhibitors of Intracellular Protein-Protein Interactions. Angew Chem Int Ed Engl. 2;54(10):2960-5.
32. Knight, Stakaityte, Abdul-Sada, Blair, Stevens, Macdonald, Blackbourn & Whitehouse. (2015). Merkel cell polyomavirus small T antigen mediates microtubule destabilisation to promote cell motility and migration. Journal of Virology. 89:35-47.
31. Muller, Prescott, Wasson & Macdonald (2015). Human papillomavirus E5 oncoprotein: function and potential target for antiviral therapeutics. Future Virology 10 (1): 27-40.
30. Stakaityte, Wood, Knight, Abdul-Sada, Azdahar, Nwogu, Macdonald & Whitehouse (2014). Merkel cell polyomavirus: insights into the most recently discovered human tumour virus. Cancers 01/2014 6(3):1267-1297.
29. Wittmann, Doble, Wasson, Richards, Haider, Bachmann, Pfeilschifter, Werfel, Muhl & Macdonald (2014). Regulation of interleukin-18 binding protein, a critical anti-inflammatory cytokine in health and infectious disease. British Journal of Dermatology. 170:E19-20.
28. Richards, Doble, Wasson, Blair, Wittmann & Macdonald (2014). Human Papillomavirus E7 Oncoprotein Increases Production of the Anti-Inflammatory Interleukin-18 Binding Protein in Keratinocytes. Journal of Virology 88(8):4173-9.
27. Griffiths, Abdul-Sada, Knight, Jackson, Richards, Prescott, Peach, Blair, Macdonald* & Whitehouse* (2013). Merkel cell polyomavirus small T antigen targets the NEMO adaptor protein to disrupt inflammatory signalling. Journal of Virology 87(24):13853-67
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