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Genetic and Epidemiological Analysis of Influenza Virus Epidemics in Taiwan during 2003 to 2006 ^,

Jhih-Wei Jian,^1, Guang-Wu Chen,^2,3, 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 Shih^3,6*

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.

Published ahead of print on 6 February 2008.

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

These authors contributed equally to this work.