Hemagglutinin and neuraminidase of a non-pathogenic H7N7 avian influenza virus coevolved during the acquisition of intranasal pathogenicity in chickens

Ichikawa, Takaya; Hiono, Takahiro; Okamatsu, Masatoshi; Maruyama, Junki; Kobayashi, Daiki; Matsuno, Keita; Kida, Hiroshi; Sakoda, Yoshihiro

Hemagglutinin and neuraminidase of a non-pathogenic H7N7 avian influenza virus coevolved during the acquisition of intranasal pathogenicity in chickens

Ichikawa, Takaya; Hiono, Takahiro; Okamatsu, Masatoshi et al.

Archives of virology, 2024, 169(10)

Permalink : https://hdl.handle.net/2115/96065

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アクセス権	open access
URI	https://hdl.handle.net/2115/96065
タイトル	Hemagglutinin and neuraminidase of a non-pathogenic H7N7 avian influenza virus coevolved during the acquisition of intranasal pathogenicity in chickens
著者	Ichikawa, Takaya ; Hiono, Takahiro ; Okamatsu, Masatoshi ; Maruyama, Junki ; Kobayashi, Daiki ; Matsuno, Keita ; Kida, Hiroshi ; Sakoda, Yoshihiro
著者名 Ichikawa, Takaya
e-Rad_Researcher 00775819 著者名 Hiono, Takahiro
e-Rad_Researcher 00507163 著者名 Okamatsu, Masatoshi
著者名 Maruyama, Junki
著者名 Kobayashi, Daiki
e-Rad_Researcher 40753306 著者名 Matsuno, Keita
e-Rad_Researcher 10109506 著者名 Kida, Hiroshi
e-Rad_Researcher 40333637 著者名 Sakoda, Yoshihiro
言語	英語
キーワード	High-pathogenicity avian influenza virus
	Intranasal pathogenicity
	Chicken
	Hemagglutinin
	Neuraminidase
発行日	2024-09-22
出版者	Springer
収録物名	Archives of virology
巻(号)	169(10)
抄録	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 degrees 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.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
権利情報	This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1007/s00705-024-06118-z
PISSN	0304-8608
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1007/s00705-024-06118-z