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Journal of Clinical Microbiology, April 2008, p. 1426-1434, Vol. 46, No. 4
0095-1137/08/$08.00+0     doi:10.1128/JCM.01560-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Genetic and Epidemiological Analysis of Influenza Virus Epidemics in Taiwan during 2003 to 2006{triangledown} ,{dagger}

Jhih-Wei Jian,1,{ddagger} Guang-Wu Chen,2,3,{ddagger} Cheng-Tsung Lai,1 Li-Ching Hsu,1 Pei-Jer Chen,4 Steve Hsu-Sung Kuo,1 Ho-Sheng Wu,1,5* and Shin-Ru Shih3,6*

Research & Diagnostic Center, Centers for Disease Control, Taipei, Taiwan, Republic of China,1 Department of Computer Science & Information Engineering,2 Research Center for Emerging Viral Infections, Chang Gung University, Taoyuan, Taiwan, Republic of China,3 Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China,4 School of Medical Laboratory Science and Biotechnology, Taipei Medical University, Taipei, Taiwan, Republic of China,5 Department of Medical Biotechnology & Laboratory Science, Chang Gung University, Taoyuan, Taiwan, Republic of China6

Received 5 August 2007/ Returned for modification 19 December 2007/ Accepted 24 January 2008

The genetic characterization of Taiwanese influenza A and B viruses on the basis of analyses of pairwise amino acid variations, genetic clustering, and phylogenetics was performed. A total of 548, 2,123, and 1,336 sequences of the HA1 genes of influenza A virus subtypes H1 and H3 and influenza B virus, respectively, collected during 2003 to 2006 from an island-wide surveillance network were determined. Influenza A virus H3 showed activity during all periods, although it was dominant only in the winters of 2002-2003 and 2003-2004. Instead, influenza B virus and influenza A virus H1 were dominant in the winters of 2004-2005 and 2005-2006, respectively. Additionally, two influenza A virus H3 peaks were found in the summers of 2004 and 2005. From clustering analysis, similar characteristics of high sequence diversity and short life spans for the influenza A virus H1 and H3 clusters were observed, despite their distinct seasonal patterns. In contrast, clusters with longer life spans and fewer but larger clusters were found among the influenza B viruses. We also noticed that more amino acid changes at antigenic sites, especially at sites B and D in the H3 viruses, were found in 2003 and 2004 than in the following 2 years. The only epidemic of the H1 viruses, which occurred in the winter of 2005-2006, was caused by two genetically distinct lineages, and neither of them showed apparent antigenic changes compared with the antigens of the vaccine strain. For the influenza B viruses, the multiple dominant lineages of Yamagata-like strains with large genetic variations observed reflected the evolutionary pressure caused by the Yamagata-like vaccine strain. On the other hand, only one dominant lineage of Victoria-like strains circulated from 2004 to 2006.

* Corresponding author. Mailing address for Shin-Ru Shih (virology questions): Department of Medical Biotechnology and Laboratory Science, Chang Gung University, 259 Wen-Hua 1st Road, Kweishan, Taoyuan, 333 Taiwan, Republic of China. Phone: 886-3-2118800, ext. 5497. Fax: 886-3-2118174. E-mail: srshih{at}mail.cgu.edu.tw. Mailing address for Ho-Sheng Wu (other questions): Research & Diagnostic Center, Centers for Disease Control, No. 161, Kun-Yang Street, Taipei, 115, Taiwan, Republic of China. Phone: 886-2-26531377. Fax: 886-2-27837779. E-mail: wuhs{at}cdc.gov.tw

{triangledown} Published ahead of print on 6 February 2008.

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

{ddagger} These authors contributed equally to this work.

Journal of Clinical Microbiology, April 2008, p. 1426-1434, Vol. 46, No. 4
0095-1137/08/$08.00+0     doi:10.1128/JCM.01560-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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