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Journal of Virology, December 2005, p. 15123-15130, Vol. 79, No. 24
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.24.15123-15130.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Clade Replacements in Dengue Virus Serotypes 1 and 3 Are Associated with Changing Serotype Prevalence{dagger}

Chunlin Zhang,1 Mammen P. Mammen Jr.,1 Piyawan Chinnawirotpisan,1 Chonticha Klungthong,1 Prinyada Rodpradit,1 Patama Monkongdee,1 Suchitra Nimmannitya,2 Siripen Kalayanarooj,2 and Edward C. Holmes3*

Department of Virology, U.S. Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand,1 Queen Sirikit National Institute of Child Health, Bangkok, Thailand,2 Center for Infectious Disease Dynamics, Department of Biology, The Pennsylvania State University, Mueller Laboratory, University Park, Pennsylvania 168023

Received 3 December 2004/ Accepted 20 September 2005

The evolution of dengue virus (DENV) is characterized by phylogenetic trees that have a strong temporal structure punctuated by dramatic changes in clade frequency. To determine the cause of these large-scale phylogenetic patterns, we examined the evolutionary history of DENV serotype 1 (DENV-1) and DENV-3 in Thailand, where gene sequence and epidemiological data are relatively abundant over a 30-year period. We found evidence for the turnover of viral clades in both serotypes, most notably in DENV-1, where a major clade replacement event took place in genotype I during the mid-1990s. Further, when this clade replacement event was placed in the context of changes in serotype prevalence in Thailand, a striking pattern emerged; an increase in DENV-1 clade diversity was associated with an increase in the abundance of this serotype and a concomitant decrease in DENV-4 prevalence, while clade replacement was associated with a decline in DENV-1 prevalence and a rise of DENV-4. We postulate that intraserotypic genetic diversification proceeds at times of relative serotype abundance and that replacement events can result from differential susceptibility to cross-reactive immune responses.

* Corresponding author. Mailing address: Center for Infectious Disease Dynamics, Department of Biology, The Pennsylvania State University, Mueller Laboratory, University Park, PA 16802. Phone: (814) 863-4689. Fax: (814) 865-9131. E-mail: ech15{at}psu.edu.

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

Journal of Virology, December 2005, p. 15123-15130, Vol. 79, No. 24
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.24.15123-15130.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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