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.
%0 Journal Article
%1 Lemey:2004uo
%A Lemey, Philippe
%A Pybus, Oliver G
%A Rambaut, Andrew
%A Drummond, Alexei J
%A Robertson, David L
%A Roques, Pierre
%A Worobey, Michael
%A Vandamme, Anne-Mieke
%C Rega Institute for Medical Research, KULeuven, B-3000 Leuven, Belgium. philippe.lemey@uz.kueluven.ac.be
%D 2004 Jul
%J Genetics
%K BEAST HIV
%N 3
%P 1059--1068
%R 10.1534/genetics.104.026666
%T The molecular population genetics of HIV-1 group O.
%U http://dx.doi.org/10.1534/genetics.104.026666
%V 167
%X 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.
@article{Lemey:2004uo,
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.},
added-at = {2009-10-13T22:05:20.000+0200},
address = {Rega Institute for Medical Research, KULeuven, B-3000 Leuven, Belgium. philippe.lemey@uz.kueluven.ac.be},
au = {Lemey, P and Pybus, OG and Rambaut, A and Drummond, AJ and Robertson, DL and Roques, P and Worobey, M and Vandamme, AM},
author = {Lemey, Philippe and Pybus, Oliver G and Rambaut, Andrew and Drummond, Alexei J and Robertson, David L and Roques, Pierre and Worobey, Michael and Vandamme, Anne-Mieke},
biburl = {https://www.bibsonomy.org/bibtex/299d8b268347324e86e39fd7b5f0a913b/ebo},
da = {20040728},
date-added = {2008-11-28 10:41:08 -0800},
date-modified = {2008-11-28 10:41:08 -0800},
dcom = {20050224},
doi = {10.1534/genetics.104.026666},
edat = {2004/07/29 05:00},
interhash = {b2c470a8cf4b111b25c240e4785c6f25},
intrahash = {99d8b268347324e86e39fd7b5f0a913b},
issn = {0016-6731 (Print)},
jid = {0374636},
journal = {Genetics},
jt = {Genetics},
keywords = {BEAST HIV},
language = {eng},
lr = {20061115},
mh = {Bayes Theorem; Cameroon; *Evolution, Molecular; *Genetics, Population; *Genome, Viral; HIV-1/*genetics; Humans; Likelihood Functions; *Models, Genetic; Phylogeny; Recombination, Genetic/genetics; Species Specificity; Viral Proteins/genetics},
mhda = {2005/02/25 09:00},
number = 3,
own = {NLM},
pages = {1059--1068},
pii = {167/3/1059},
pl = {United States},
pmc = {PMC1470933},
pmid = {15280223},
pst = {ppublish},
pt = {Comparative Study; Journal Article; Research Support, Non-U.S. Gov't},
pubm = {Print},
rn = {0 (Viral Proteins)},
sb = {IM},
so = {Genetics. 2004 Jul;167(3):1059-68.},
stat = {MEDLINE},
timestamp = {2009-10-13T22:05:20.000+0200},
title = {The molecular population genetics of HIV-1 group O.},
url = {http://dx.doi.org/10.1534/genetics.104.026666},
volume = 167,
year = {2004 Jul}
}