Increase of GII.2 norovirus infections during the 2009-2010 season in Osaka City, Japan

被引:57
作者
Iritani, Nobuhiro [1 ]
Kaida, Atsushi [1 ]
Abe, Niichiro [1 ]
Sekiguchi, Jun-ichiro [1 ]
Kubo, Hideyuki [1 ]
Takakura, Koh-Ichi [2 ]
Goto, Kaoru [1 ]
Ogura, Hisashi [3 ]
Seto, Yoshiyuki [4 ]
机构
[1] Osaka City Inst Publ Hlth & Environm Sci, Dept Microbiol, Tennoji Ku, Osaka 5430026, Japan
[2] Osaka City Inst Publ Hlth & Environm Sci, Dept Urban Environm, Tennoji Ku, Osaka 5430026, Japan
[3] Osaka City Univ, Sch Med, Dept Virol, Abeno Ku, Osaka 545, Japan
[4] Osaka Prefecture Univ, Microbiol Lab, Dept Vet Sci, Grad Sch Life & Environm Sci, Izumisano, Osaka, Japan
关键词
evolution; genotyping; molecular surveillance; outbreak; recombination; viral gastroenteritis; NORWALK-LIKE VIRUSES; MOLECULAR EPIDEMIOLOGY; UNITED-STATES; GASTROENTERITIS; OUTBREAKS; STRAIN; IDENTIFICATION; SEQUENCE;
D O I
10.1002/jmv.23211
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
During the 20092010 season, a significant numerical increase of genotype GII.2 norovirus (NoV)-associated outbreaks was observed in Osaka City, Japan. The most common genotype in that season was GII.2 (44.6%), followed by GII.4 (39.2%). Mostly, GII.2 strains were associated with outbreaks in children and with person-to-person contact. The National Infectious Disease Surveillance Center reported that GII.2 NoV infections were widespread in Japan in that season. Comparative phylogenetic analysis of RNA-dependent RNA polymerase (RdRp) and capsid sequences revealed that this GII.2 epidemic resulted from two genetic strains. The first, GII.2p2 strains, had an identical genotype in the RdRp and capsid genes. GII.2p2 strains in the 20092010 season were a different genetic cluster from the strains of spring 2004, the previous epidemic of GII.2 NoV, but showed no unique amino acid change. The second, GII.2 chimera virus (GII.2p16), had GII.16 RdRp and GII.2 capsid genotypes, suggesting prior recombination at the junction of ORF1 and ORF2. GII.2p16 strains had four significant amino acid changes in the P2 subdomain, suggesting antigenic changes. Before the 20092010 season, GII.2 chimera viruses had been observed only sporadically. This spreading of GII.2p16 strains in the 20092010 season might be the first epidemic of GII.2 chimera virus. This study revealed that the NoV epidemic in the 20092010 season differed considerably from the prior season, when GII.4 was predominant. Furthermore, GII.2 strains persisted in human populations by drastic recombination and gradual accumulation of mutations, indicating a prevalent pattern of non-GII.4 genotypes with genetic evolution. J. Med. Virol. 84:517525, 2012. (C) 2011 Wiley Periodicals, Inc.
引用
收藏
页码:517 / 525
页数:9
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