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Hemagglutinin and neuraminidase of a non-pathogenic H7N7 avian influenza virus coevolved during the acquisition of intranasal pathogenicity in chickens.
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- Author(s): Ichikawa T;Ichikawa T;Ichikawa T; Hiono T; Hiono T; Hiono T; Hiono T; Hiono T; Okamatsu M; Okamatsu M; Maruyama J; Maruyama J; Maruyama J; Kobayashi D; Kobayashi D; Matsuno K; Matsuno K; Matsuno K; Matsuno K; Kida H; Kida H; Kida H; Sakoda Y; Sakoda Y; Sakoda Y; Sakoda Y; Sakoda Y
- Source:
Archives of virology [Arch Virol] 2024 Sep 22; Vol. 169 (10), pp. 207. Date of Electronic Publication: 2024 Sep 22.- Publication Type:
Journal Article- Language:
English - Source:
- Additional Information
- Source: Publisher: Springer-Verlag Country of Publication: Austria NLM ID: 7506870 Publication Model: Electronic Cited Medium: Internet ISSN: 1432-8798 (Electronic) Linking ISSN: 03048608 NLM ISO Abbreviation: Arch Virol Subsets: MEDLINE
- Publication Information: Original Publication: Wien, New York, Springer-Verlag.
- Subject Terms: Chickens*/virology ; Neuraminidase*/genetics ; Neuraminidase*/metabolism ; Influenza in Birds*/virology ; Hemagglutinin Glycoproteins, Influenza Virus*/genetics ; Hemagglutinin Glycoproteins, Influenza Virus*/metabolism ; Influenza A Virus, H7N7 Subtype*/pathogenicity ; Influenza A Virus, H7N7 Subtype*/genetics; Animals ; Virulence ; Evolution, Molecular ; Mutation ; Poultry Diseases/virology ; Viral Proteins/genetics ; Viral Proteins/metabolism
- Abstract: Polybasic amino acid residues at the hemagglutinin (HA) cleavage site are insufficient to induce the highly pathogenic phenotype of avian influenza viruses in chickens. In our previous study, an H7N7 avian influenza virus named "Vac2sub-P0", which is nonpathogenic despite carrying polybasic amino acids at the HA cleavage site, was passaged in chick air sacs, and a virus with high intravenous pathogenicity, Vac2sub-P3, was obtained. Intranasal infection with Vac2sub-P3 resulted in limited lethality in chickens; therefore, in this study, this virus was further passaged in chicken lungs, and the resultant virus, Vac2sub-P3L4, acquired high intranasal pathogenicity. Experimental infection of chickens with recombinant viruses demonstrated that mutations in HA and neuraminidase (NA) found in consecutive passages were responsible for the increased pathogenicity. The HA and NA functions of Vac2sub-P3L4 were compared with those of the parental virus in vitro; the virus growth at 40 °C was faster, the binding affinity to a sialic acid receptor was lower, and the rate of release by NA from the cell surface was lower, suggesting that these changes enabled the virus to replicate efficiently in chickens with high intranasal pathogenicity. This study demonstrates that viruses that are highly pathogenic when administered intranasally require additional adaptations for increased pathogenicity to be highly lethal to intranasally infected chickens.
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- Contributed Indexing: Keywords: Chicken; Hemagglutinin; High-pathogenicity avian influenza virus; Intranasal pathogenicity; Neuraminidase
- Accession Number: EC 3.2.1.18 (Neuraminidase)
0 (Hemagglutinin Glycoproteins, Influenza Virus)
0 (Viral Proteins) - Publication Date: Date Created: 20240922 Date Completed: 20240922 Latest Revision: 20241015
- Publication Date: 20241016
- Accession Number: 10.1007/s00705-024-06118-z
- Accession Number: 39307848
- Source:
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