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MBE Advance Access published online on January 19, 2005
Molecular Biology and Evolution, doi:10.1093/molbev/msi088
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Molecular Biology and Evolution © Society for Molecular Biology and Evolution 2005; all rights reserved.
Accepted January 3, 2005

Letter

High Copy Number in Human Endogenous Retrovirus (HERV) Families is Associated with Copying Mechanisms in Addition to Re-Infection

Robert Belshaw 1*, Aris Katzourakis 1, Jan Paces 2, Austin Burt 1, and Michael Tristem 1

1 Department of Biological Sciences, Imperial College, Silwood Park Campus, Ascot, Berks SL5 7PY, UK
2 Institute of Molecular Genetics, Academy of Sciences, Prague 6, CZ-16637, Czech Republic

* To whom correspondence should be addressed.
Robert Belshaw, E-mail: r.belshaw{at}imperial.ac.uk


  Abstract

There are at least 31 families of human endogenous retroviruses (HERVs), each derived from an independent infection by an exogenous virus. Using evidence of purifying selection on HERV genes, we have shown previously that re-infection by replication-competent elements was the predominant mechanism of copying in some families. Here we analyse the evolution of 17 HERV families using dN/dS ratios and find a positive relationship between copy number and the use of additional copying mechanisms. All families with more than 200 elements have also used one or more of the following mechanisms: (a) complementation in trans (elements copied by other elements of the same family; HERV-H and ERV-9), (b) retrotransposition in cis (elements copying themselves) within germ-line cells (HERV-K(HML3)), and (c) being copied by non-HERV machinery (HERV-W). We discuss why these other mechanisms are rare in most families and suggest why complementation in trans is significant only in the larger families.

Keywords: human; endogenous; retrovirus; infection; retrotransposition; complementation.
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