The Molecular Population Genetics of HIV-1 Group O (original) (raw)
Journal Article
Rega Institute for Medical Research
, KULeuven, B-3000 Leuven, Belgium
Corresponding author: Rega Institute for Medical Research, Minderbroedersstraat 10, B-3000 Leuven, Belgium. E-mail: [email protected]
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Department of Zoology
, University of Oxford, Oxford OX1 3PS, United Kingdom
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Department of Zoology
, University of Oxford, Oxford OX1 3PS, United Kingdom
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Department of Zoology
, University of Oxford, Oxford OX1 3PS, United Kingdom
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School of Biological Sciences
, University of Manchester, Manchester M13 9PT, United Kingdom
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Service de Neurovirologie
, CEA, 92260 Fontenay-aux-Roses, France
Service de Neurovirologie
, CIRMF, BP 769 Franceville, Gabon
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Department of Ecology and Evolutionary Biology
, University of Arizona, Tucson Arizona 85721
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Rega Institute for Medical Research
, KULeuven, B-3000 Leuven, Belgium
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Received:
21 January 2004
Cite
Philippe Lemey, Oliver G Pybus, Andrew Rambaut, Alexei J Drummond, David L Robertson, Pierre Roques, Michael Worobey, Anne-Mieke Vandamme, The Molecular Population Genetics of HIV-1 Group O, Genetics, Volume 167, Issue 3, 1 July 2004, Pages 1059–1068, https://doi.org/10.1534/genetics.104.026666
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Abstract
HIV-1 group O originated through cross-species transmission of SIV from chimpanzees to humans and has established a relatively low prevalence in Central Africa. Here, we infer the population genetics and epidemic history of HIV-1 group O from viral gene sequence data and evaluate the effect of variable evolutionary rates and recombination on our estimates. First, model selection tools were used to specify suitable evolutionary and coalescent models for HIV group O. Second, divergence times and population genetic parameters were estimated in a Bayesian framework using Markov chain Monte Carlo sampling, under both strict and relaxed molecular clock methods. Our results date the origin of the group O radiation to around 1920 (1890–1940), a time frame similar to that estimated for HIV-1 group M. However, group O infections, which remain almost wholly restricted to Cameroon, show a slower rate of exponential growth during the twentieth century, explaining their lower current prevalence. To explore the effect of recombination, the Bayesian framework is extended to incorporate multiple unlinked loci. Although recombination can bias estimates of the time to the most recent common ancestor, this effect does not appear to be important for HIV-1 group O. In addition, we show that evolutionary rate estimates for different HIV genes accurately reflect differential selective constraints along the HIV genome.
© Genetics 2004
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