1. Defect of rabies virus phosphoprotein in its interferon-antagonist activity negatively affects viral replication in muscle cells
- Author
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Kota Okadera, Kento Nakagawa, Makoto Sugiyama, Hiromichi Mitake, Kazuma Okada, Naoto Ito, and Satoko Yamaoka
- Subjects
0301 basic medicine ,Rabies ,Biology ,Virus Replication ,medicine.disease_cause ,Cell Line ,Mice ,Viral Proteins ,03 medical and health sciences ,Interferon ,medicine ,Animals ,Myocyte ,Muscle Cells ,Virulence ,General Veterinary ,Rabies virus ,Antagonist ,interferon antagonist ,Phosphoproteins ,Note ,phosphoprotein ,Virology ,Molecular biology ,030104 developmental biology ,Viral replication ,Phosphoprotein ,biology.protein ,Interferons ,Public Health ,Antibody ,Antagonism ,medicine.drug - Abstract
Attenuated derivative rabies virus Ni-CE replicates in muscle cells less efficiently than does the parental pathogenic strain Nishigahara. To examine the mechanism underlying the less efficient replication of Ni-CE, we compared the activities of Ni-CE and Nishigahara phosphoproteins, viral interferon (IFN) antagonists, to suppress IFN-β promoter activity in muscle cells and we demonstrated a defect of Ni-CE phosphoprotein in this ability. Treatment with an IFN-β-neutralizing antibody improved the replication efficiency of Ni-CE in muscle cells, indicating that produced IFN inhibits Ni-CE replication. The results indicate the importance of IFN antagonism of rabies virus phosphoprotein for viral replication in muscle cells.
- Published
- 2017
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