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Professor George Brownlee, FRS

Professor George Brownlee, FRS

Academic Profile
I was educated in Cambridge, at Emmanuel College, where I held a Research Fellowship gaining my PhD in 1967 studying under Dr Fred Sanger at the Laboratory of Molecular Biology, Cambridge. I remained in Cambridge as a permanent member of staff of the Medical Research Council until 1980. I then took up my appointment as the first holder of the E.P. Abraham Professor of Chemical Pathology at the Sir William Dunn School of Pathology in Oxford University, which I have held since then, in conjunction with a Fellowship at Lincoln College. I was elected a Fellow of the Royal Society in 1987.

Research Interests
My early research interests in Cambridge were in Molecular Biology - a field of enquiry that rapidly expanded in the 1970s. Since I was interested in sequencing RNA and DNA, it was possible to make fundamental discoveries quite easily as so little was known then about genes. My group made several early discoveries. For example, in 1977, we discovered the existence of pseudogenes- abnormal, mutated genes, now known to be ubiquitous in the genome of all organisms.

Since 1980, I have been interested in applying molecular techniques to more applied medical problems. In 1982, my group were the first to isolate the clotting factor IX gene - a gene defective in patients with a rare, inherited disease, haemophilia B. Our pioneering work was subsequently developed by the pharmaceutical industry and is the basis of a recombinant factor IX protein preparation now used to treat patients with haemophilia B. We are now studying gene regulation in influenza virus - another medically important disease. Our present interest is to understand the difficult problem of how the segmented RNA gene is copied in a regulated manner. This work may have implications for the development of novel influenza vaccines in the future. Details of our current research and publications is available under research/George Brownlee on

Research publications, achievements etc 6/2000-6/2001
We have continued our interest in the gene regulation of influenza virus genome publishing 9 papers and reviews within the year. Perhaps our most significant paper is the data suggesting that influenza virus replication may occur in close proximity to the host RNA polymerase II within the nucleus of the infected cell. With a colleague, Dr E. Fodor we have written an up-to-date review of influenza virus replication.



  • Poon LLM, Fodor E and Brownlee GG (2000). Polyuridylated mRNA synthesized by a recombinant influenza virus is defective in nuclear export. J. Virology 74: 418-427.
  • Solorzano A, Zheng H, Fodor E, Brownlee GG, Palese P and García-Sastre A (2000). Reduced levels of neuraminidase of influenza A viruses correlate with attenuated phenotypes in mice. J. Gen. Virology 81: 737-742.
  • Fodor E, Mikulásová A, Mingay LJ, Poon LLM and Brownlee GG (2000). Messenger RNAs that are not synthesised by RNA polymerase II can be 3' end cleaved and polyadenylated. EMBO Reports, 1: 513-518.
  • Leahy MB, Pritlove DC, Poon LLM and Brownlee GG (2001). Mutagenic analysis of the 5' arm of the influenza A virus virion RNA promoter defines the sequence requirements for endonuclease activity. J. Virology, 75: 134-142.
  • Leahy MB, Dobbyn HC and Brownlee GG (2001). A hairpin loop structure in the 3' arm of the influenza A virus virion RNA promoter is required for endonuclease activity. J. Virology 75: 7042-7049.
  • Brownlee GG and Giangrande PLF (2001). Clotting Factors VIII and IX. In Recombinant Protein Drugs, pp 67-88 (P Buckel, ed) Birkhauser, Basel.
  • Fodor E and Brownlee GG (2001). Influenza virus replication (review). In "Perspectives in Medical Virology" (Zuckerman AJ and Mushawar LK eds) Elsevier Science, Amsterdam, in press.
  • Fodor E, Poon LLM, Mikulasova A, Mingay LJ and Brownlee GG (2001). Transcription of influenza virus genes. In "Options for the Control of Influenza IV" (Osterhaus, ADME et al,Eds) Elsevier Science, Amsterdam, in press.
  • Brownlee GG and Fodor E (2001). Predicted antigenicity of the 1918 Spanish influenza suggests an avian origin. Phil. Trans. Roy. Soc. Lond., in press.

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