This Article Full Text Full Text (PDF) Other Versions of this Article: JVI.02683-07v1 82/10/4807    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Google Scholar Articles by Boni, M. F. Articles by Holmes, E. C. PubMed PubMed Citation Articles by Boni, M. F. Articles by Holmes, E. C.

 Previous Article  |  Next Article 

Journal of Virology, May 2008, p. 4807-4811, Vol. 82, No. 10
0022-538X/08/$08.00+0     doi:10.1128/JVI.02683-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Homologous Recombination Is Very Rare or Absent in Human Influenza A Virus

Resources for the Future, Washington, District of Columbia 20036,¹ Department of Ecology and Evolutionary Biology, Princeton University, Princeton, New Jersey 08544,² Center for Infectious Disease Dynamics, Department of Biology, The Pennsylvania State University, State College, Pennsylvania 16802,³ Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892,⁴ Fogarty International Center, National Institutes of Health, Bethesda, Maryland 20892⁵

Received 18 December 2007/ Accepted 26 February 2008

To determine the extent of homologous recombination in human influenza A virus, we assembled a data set of 13,852 sequences representing all eight segments and both major circulating subtypes, H3N2 and H1N1. Using an exhaustive search and a nonparametric test for mosaic structure, we identified 315 sequences (2%) in five different RNA segments that, after a multiple-comparison correction, had statistically significant mosaic signals compatible with homologous recombination. Of these, only two contained recombinant regions of sufficient length (>100 nucleotides [nt]) that the occurrence of homologous recombination could be verified using phylogenetic methods, with the rest involving very short sequence regions (15 to 30 nt). Although this secondary analysis revealed patterns of phylogenetic incongruence compatible with the action of recombination, neither candidate recombinant was strongly supported. Given our inability to exclude the occurrence of mixed infection and template switching during amplification, laboratory artifacts provide an alternative and likely explanation for the occurrence of phylogenetic incongruence in these two cases. We therefore conclude that, if it occurs at all, homologous recombination plays only a very minor role in the evolution of human influenza A virus.

Published ahead of print on 19 March 2008.

This article has been cited by other articles:

• Krasnitz, M., Levine, A. J., Rabadan, R. (2008). Anomalies in the Influenza Virus Genome Database: New Biology or Laboratory Errors?. J. Virol. 82: 8947-8950 [Abstract] [Full Text]