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Journal of Virology, September 2006, p. 8503-8509, Vol. 80, No. 17
0022-538X/06/$08.00+0     doi:10.1128/JVI.00585-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Phylogenetic Analysis Reveals a Correlation between the Expansion of Very Virulent Infectious Bursal Disease Virus and Reassortment of Its Genome Segment B

Chung-Chau Hon,1 Tsan-Yuk Lam,1 Alexei Drummond,2 Andrew Rambaut,3 Yiu-Fai Lee,4 Chi-Wai Yip,1 Fanya Zeng,1 Pui-Yi Lam,1 Patrick T. W. Ng,4 and Frederick C. C. Leung1*

Department of Zoology, The University of Hong Kong, Hong Kong, China,1 Department of Computer Science, University of Auckland, Auckland, New Zealand,2 Department of Zoology, The University of Oxford, Oxford, United Kingdom,3 Department of Mathematics, The University of Hong Kong, Hong Kong, China4

Received 23 March 2006/ Accepted 7 June 2006

Infectious bursal disease virus (IBDV) is a birnavirus causing immunosuppressive disease in chickens. Emergence of the very virulent form of IBDV (vvIBDV) in the late 1980s dramatically changed the epidemiology of the disease. In this study, we investigated the phylogenetic origins of its genome segments and estimated the time of emergence of their most recent common ancestors. Moreover, with recently developed coalescence techniques, we reconstructed the past population dynamics of vvIBDV and timed the onset of its expansion to the late 1980s. Our analysis suggests that genome segment A of vvIBDV emerged at least 20 years before its expansion, which argues against the hypothesis that mutation of genome segment A is the major contributing factor in the emergence and expansion of vvIBDV. Alternatively, the phylogeny of genome segment B suggests a possible reassortment event estimated to have taken place around the mid-1980s, which seems to coincide with its expansion within approximately 5 years. We therefore hypothesize that the reassortment of genome segment B initiated vvIBDV expansion in the late 1980s, possibly by enhancing the virulence of the virus synergistically with its existing genome segment A. This report reveals the possible mechanisms leading to the emergence and expansion of vvIBDV, which would certainly provide insights into the scope of surveillance and prevention efforts regarding the disease.

* Corresponding author. Mailing address: Department of Zoology, Kadoorie Biological Science Building, The University of Hong Kong, Hong Kong, China. Phone: (852) 2299-0825. Fax: (852) 2857-4672. E-mail: fcleung{at}hkucc.hku.hk.

Journal of Virology, September 2006, p. 8503-8509, Vol. 80, No. 17
0022-538X/06/$08.00+0     doi:10.1128/JVI.00585-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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