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Journal of Clinical Microbiology, February 2009, p. 352-357, Vol. 47, No. 2
0095-1137/09/$08.00+0 doi:10.1128/JCM.01357-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Microbiology, Kobe Institute of Health, 4-6, Minatojima-nakamachi, Chuo-ku, Kobe 650-0046, Japan,1 Department of Infectious Control, Osaka Medical College Hospital, 2-7, Daigaku-cho, Takatsuki 569-8686, Japan2
Received 16 July 2008/ Returned for modification 1 November 2008/ Accepted 8 December 2008
In the 2004-2005 season, there was a large epidemic of the influenza B virus Yamagata group in Kobe, Japan. In hemagglutination inhibition tests, most of the clinical isolates from Kobe showed antigenicities similar to those of previous isolates (the vaccine-type virus). Only a few antigenic variants were isolated around the peak of the epidemic; however, Kobe residents developed antibodies against the variants during the season. The antigenic variants showed a one-point mutation of a nucleotide in the HA1 gene (C440A or G421A), which resulted in the substitution of one amino acid in the 150 loop of the HA molecule (T147N or G141R). The 150 loop is one of four epitopes of the hemagglutinin molecule of the influenza B virus. We established a system to detect one-point differences in the nucleotides of the 150 loop by means of high-resolution melting curve analysis with LCGreen. With this system, the isolates were determined to be the vaccine-type virus, antigenic variants, or a mixture of both. Some isolates were shown to be mixtures although they had been recognized as the vaccine-type virus with the hemagglutination inhibition tests. Thus, the antigenic variants appeared in the early period of the epidemic and were cocirculating with the vaccine-type virus during the epidemic.
Published ahead of print on 17 December 2008.
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