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Journal of Virology, September 2007, p. 9437-9442, Vol. 81, No. 17
0022-538X/07/$08.00+0     doi:10.1128/JVI.02216-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Rate of Recombinational Deletion among Human Endogenous Retroviruses{triangledown}

Robert Belshaw,1* Jason Watson,2 Aris Katzourakis,1 Alexis Howe,1,2 John Woolven-Allen,2,3 Austin Burt,2 and Michael Tristem2

Department of Zoology, University of Oxford, Oxford OX1 3PS,1 Division of Biology, Imperial College London, Silwood Park Campus, Ascot, Berkshire Sl5 7PY,2 Plymouth Marine Laboratory, Prospect Place, The Hoe, Plymouth PL1 3DH, United Kingdom3

Received 9 October 2006/ Accepted 12 June 2007

The fate of most human endogenous retroviruses (HERVs) has been to undergo recombinational deletion. This process involves homologous recombination between the flanking long terminal repeats (LTRs) of a full-length element, leaving a relic structure in the genome termed a solo LTR. We examined loci in one family, HERV-K(HML2), and found that the deletion rate decreased markedly with age: the rate among recently integrated loci was almost 200-fold higher than that among loci whose insertion predated the divergence of humans and chimpanzees (8 x 10–5 and 4 x 10–7 recombinational deletion events per locus per generation, respectively). One hypothesis for this finding is that increasing mutational divergence between the flanking LTRs reduces the probability of homologous recombination and thus the rate of solo LTR formation. Consistent with this idea, we were able to replicate the observed rates by a simulation in which the probability of recombinational deletion was reduced 10-fold by a single mutation and 100-fold by any additional mutations. We also discuss the evidence for other factors that may influence the relationship between locus age and the rate of deletion, for example, host recombination rates and selection, and highlight the consequences of recombinational deletion for dating recent HERV integrations.


* Corresponding author. Mailing address: Department of Zoology, University of Oxford, Oxford OX1 3PS, United Kingdom. Phone: 44 1865 281997. Fax: 44 1865 271249. E-mail: robert.belshaw{at}zoo.ox.ac.uk

{triangledown} Published ahead of print on 20 June 2007.


Journal of Virology, September 2007, p. 9437-9442, Vol. 81, No. 17
0022-538X/07/$08.00+0     doi:10.1128/JVI.02216-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




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