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Nelson Bay Orthoreovirus cell attachment protein σC determines strain-specific differences in infectivity and
Takahiro Kawagishi1, Yusuke Sakai2, Hiroya Oki3,4
1Department of Virology, Research Institute for Microbial Diseases (RIMD), The University of Osaka, Osaka, Japan.
Plos Pathogens
|August 3, 2026
Summary
Nelson Bay orthoreovirus (NBV) can infect humans, but its virulence mechanisms are unclear. The S1 gene segment, specifically the σC protein
Area of Science:
- Virology
- Pathogenesis
- Molecular Biology
Background:
- Nelson Bay orthoreovirus (NBV) is increasingly isolated from human respiratory infections.
- NBV transmission and disease mechanisms in humans require elucidation.
- Previous studies identified fusion-associated small transmembrane (FAST) protein and σC as important for NBV Miyazaki-Bali/2007 (MB) strain virulence.
Purpose of the Study:
- To compare the virulence of NBV strains from human (MB) and bat (NelB) origins.
- To identify the NBV genetic determinants responsible for strain-specific virulence.
- To elucidate the role of S1 gene segment proteins in NBV pathogenesis.
Main Methods:
- Comparative virulence assessment in a mouse model.
- Reverse genetics to construct and analyze NBV reassortant viruses.
- Site-directed mutagenesis of the σC protein.
Main Results:
- The NelB strain exhibited significantly lower virulence than the MB strain in mice.
- The S1 gene segment was identified as a key determinant of NBV virulence.
- The viral structural protein σC, encoded by S1, was responsible for the observed virulence differences.
- The middle body domain of σC, not the putative receptor-binding domain, mediated differential virulence.
Conclusions:
- The S1 gene segment, particularly the σC protein, dictates NBV strain virulence.
- NBV pathogenesis involves specific domains within the σC protein.
- These findings advance understanding of NBV transmission and disease mechanisms.
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