C.V.
| Year |
Description |
2003 – 2007 |
Head of Institute, IEB |
2006 |
Elected Fellow of the Royal Society of Edinburgh |
2000 – 2002 |
Visiting Professor, Department of Pathology, University of California San Diego |
1998 – present |
Professor of Evolutionary Genetics, University of Edinburgh |
1992 – 2000 |
Convenor, Centre for HIV Research, University of Edinburgh |
1992 – 1998 |
Reader, Institute of Cell, Animal and Population Biology |
1984 – 1992 |
Lecturer, Department of Genetics, University of Edinburgh |
1982 – 1984 |
SERC Advanced Fellow, School of Biological Sciences, University of Sussex |
1979 – 1982 |
Research Fellow , Imperial Cancer Research Fund, London |
1977 – 1978 |
Visiting Fellow, National Institute of Environmental Health Sciences, (NIH), North Carolina, U.S.A. |
1976 |
PhD; Department of Genetics, University of Leicester |
1973 |
BSc (Hons) Zoology University College London |
Research groupings
Population Genetics
Genetics of Complex Traits
Evolution and Infection
Teaching
Undergraduate
Evolution in Action 2 (BI0012)
Evolutionary and Ecological Genetics 3 (IP0002)
Honours Modules: Molecular and Cellular Basis of HIV Infection (U00682); Molecular Phylogenetics (U03444)
Postgraduate
Programme Director: MSc in Quantitative Genetics and Genome Analysis
Research interests
My area of research is the analysis of genetic variation and evolution of HIV, particularly the evolution of drug resistance. I returned from an appointment as a Visiting Professor at the University of California San Diego in 2002 and retain close links with collegues there.
In current research in Edinburgh we are studying using statistical and machine learning approaches to study the genetic basis of combination antiretroviral drug resistance in HIV and influenza. This work is currently supported by the BBSRC.
I am also analyzing factors influencing transmission of drug resistant strains of HIV, and modelling their future spread. Using HIV sequences obtained in the course of clinical treatment we are able to reconstruct the recent HIV epidemic in the UK to understand the temporal patterns of sexual transmission. This involves collaborations with colleagues in London and elsewhere as part of a UK-wide multicentre study of the drug resistance as a determinant of clinical response to antiretroviral therapy. This work is supported by the Medical Research Council.
For several years we have also been interested in the population genetics of HIV within infected patients and the factors influencing the pattern of mutations conferring drug resistance. This has recently extended to studies of CTL-mediated selection using codon-based models, especially in the coding regions of HIV-1 protease and reverse transcriptase. This work is supported by the NIH.
Representative publications
Murray RJ, Lewis F., Miller, MD, Leigh Brown AJ. Genetic basis of variation in tenofovir drug susceptibility. AIDS 2008 (in press).
Lewis F, Hughes GJ, Rambaut A, Pozniak A, Leigh Brown AJ. Episodic Sexual Transmission of HIV Revealed by Molecular Phylodynamics. PLoS Med., 2008, 5: e50.
Pillay D, Rambaut A, Geretti AM, Leigh Brown AJ. HIV phylogenetics. BMJ 2007; 335: 460-1.
Poon A.F.Y., Kosakovsky Pond S.L., Bennett P., Richman D.D., Leigh Brown A.J., Frost, S.D.W. Adaptation to human populations is revealed by within-host polymorphisms in HIV-1 and hepatitis C virus. PLoS Pathog 3(3), 2007: e45.
Kosakovsky Pond SL, Frost SDW, Grossman Z, Gravenor MB, Richman DD, Leigh Brown AJ. Adaptation to different human populations by HIV-1 revealed by codon-based analyses. PLoS Comput Biol. 2; e62, 2006.
Yang, O.O., Daar, E.S., Jamieson, B.D., Balamururugam, A., Smith, D.M., Pitt, J.A., Petropoulos, C.J., Richman, D.D., Little, S.J. and Leigh Brown A.J. HIV-1 Clade B superinfection: evidence for differential immune containment of distinct clade B strains. J. Virol. 79, 860-868, 2005.
Froebel, K. Howard, W., Schafer, J., Howie, F., Whitworth, J., Kaleebu, P., Leigh Brown, A. and Riley, E. Activation by malaria antigenes renders mononuclear cells susceptible to HIV infection and reactivates replication of endogenous HIV in cells from HIV infected donors. Parasite Immunol. 26, 213-217, 2004
Leigh Brown, A.J., Frost, S.D.W., Good, B., Daar, E.S., Simon, V., Markowitz, M., Collier, A.C., Connick, E., Conway, B., Margolick, J.B., Routy, J-P., Corbeil, J., Hellmann, N.S., Richman, D.D., Little, S.J. Genetic basis of hypersusceptibility to protease inhibitors and low replicative capacity of Human Immunodeficiency Virus Type strains in primary infection. J. Virol. 78, 2242-2246, 2004
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