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1 Department of Virology II, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashi-Murayama, Tokyo 208-0011, Japan
2 Sakai Institute of Public Health, Sakai, Osaka 590-0953, Japan
3 Laboratory of Virology, Aichi Prefectural Institute of Public Health, 7-6 Nagare, Tujimachi, Kita-ku, Nagoya 462-8576, Japan
4 Saitama Institute of Public Health, Kamiokubo 639-1, Sakura-ku, Saitama 338-0824, Japan
5 Public Health and Environment Research Division, Mie Pref. Science and Technology Promotion Center, Sakuramachi 3690-1, Yokaichi, Mie 512-1211, Japan
6 Division of Virology, Chiba Prefectural Institute of Public Health, Chiba, Chiba 260-8715, Japan
7 Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-1, Gakuen-Cho, Sasai, Osaka 599-8531, Japan
8 Technical Marketing Department, Denka-Seiken Co. Ltd, 1-2-2 Minami-honcho, Gosen, Niigata 959-1695, Japan
9 Department of Pathology, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashi-Murayama, Tokyo 208-0011, Japan
Correspondence
Grant S. Hansman
ghansman{at}nih.go.jp
Naokazu Takeda
ntakeda{at}nih.go.jp
Human norovirus (NoV) strains cause a considerable number of outbreaks of gastroenteritis worldwide. Based on their capsid gene (VP1) sequence, human NoV strains can be grouped into two genogroups (GI and GII) and at least 14 GI and 17 GII genotypes (GI/1–14 and GII/1–17). Human NoV strains cannot be propagated in cell-culture systems, but expression of recombinant VP1 in insect cells results in the formation of virus-like particles (VLPs). In order to understand NoV antigenic relationships better, cross-reactivity among 26 different NoV VLPs was analysed. Phylogenetic analyses grouped these NoV strains into six GI and 12 GII genotypes. An antibody ELISA using polyclonal antisera raised against these VLPs was used to determine cross-reactivity. Antisera reacted strongly with homologous VLPs; however, a number of novel cross-reactivities among different genotypes was observed. For example, GI/11 antiserum showed a broad-range cross-reactivity, detecting two GI and 10 GII genotypes. Likewise, GII/1, GII/10 and GII/12 antisera showed a broad-range cross-reactivity, detecting several other distinct GII genotypes. Alignment of VP1 amino acid sequences suggested that these broad-range cross-reactivities were due to conserved amino acid residues located within the shell and/or P1-1 domains. However, unusual cross-reactivities among different GII/3 antisera were found, with the results indicating that both conserved amino acid residues and VP1 secondary structures influence antigenicity.
The GenBank/EMBL/DDBJ accession numbers of the sequences reported in this paper are AB081723, AB058547, DQ093065, AB195225, DQ093062, DQ093066, DQ093063, AB195226, DQ093064, AB039780, AY237414 and DQ093067.
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