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Journal of Virology, December 2005, p. 14680-14687, Vol. 79, No. 23
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.23.14680-14687.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Invasion and Maintenance of Dengue Virus Type 2 and Type 4 in the Americas{dagger}

Christine V. F. Carrington,1* Jerome E. Foster,1 Oliver G. Pybus,2 Shannon N. Bennett,3 and Edward C. Holmes4

Department of Pre-Clinical Sciences, Faculty of Medical Sciences, University of the West Indies, St. Augustine, Trinidad, West Indies,1 Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, United Kingdom,2 Asia-Pacific Institute of Tropical Medicine and Infectious Diseases, Department of Tropical Medicine, University of Hawaii, 3675 Kilauea Ave., Honolulu, Hawaii 96816,3 Center for Infectious Disease Dynamics, Department of Biology, The Pennsylvania State University, Mueller Laboratory, University Park, Pennsylvania 168024

Received 26 May 2005/ Accepted 2 September 2005

Dengue virus type 4 (DENV-4) was first reported in the Americas in 1981, where it caused epidemics of dengue fever throughout the region. In the same year, the region's first epidemic of dengue hemorrhagic fever was reported, caused by an Asian strain of dengue virus type 2 (DENV-2) that was distinct from the American subtype circulating previously. Despite the importance of these epidemics, little is known about the rates or determinants of viral spread among island and mainland populations or their directions of movement. We employed a Bayesian coalescent approach to investigate the transmission histories of DENV-2 and DENV-4 since their introduction in 1981 and a parsimony method to assess patterns of strain migration. For both viruses there was an initial invasion phase characterized by an exponential increase in the number of DENV lineages, after which levels of genetic diversity remained constant despite reported fluctuations in DENV-2 and DENV-4 activity. Strikingly, viral lineage numbers increased far more rapidly for DENV-4 than DENV-2, indicative of a more rapid rate of exponential population growth in DENV-4 or a higher rate of geographic dispersal, allowing this virus to move more effectively among localities. We propose that these contrasting dynamics may reflect underlying differences in patterns of host immunity. Despite continued gene flow along particular transmission routes, the overall extent of viral traffic was less than expected under panmixis. Hence, DENV in the Americas has a clear geographic structure that maintains viral diversity between outbreaks.

* Corresponding author. Mailing address: Department of Pre-Clinical Sciences, Faculty of Medical Sciences, University of the West Indies, St. Augustine, Trinidad. Phone and fax: (868) 662-1873. E-mail: ccarrington{at}fms.uwi.tt.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, December 2005, p. 14680-14687, Vol. 79, No. 23
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.23.14680-14687.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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