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Article: The PB2 mutation with lysine at 627 enhances the pathogenicity of avian influenza (H7N9) virus which belongs to a non-zoonotic lineage

TitleThe PB2 mutation with lysine at 627 enhances the pathogenicity of avian influenza (H7N9) virus which belongs to a non-zoonotic lineage
Authors
Issue Date2017
PublisherNature Publishing Group: Open Access Journals. The Journal's web site is located at http://www.nature.com/srep/index.html
Citation
Scientific Reports, 2017, v. 7 n. 1, p. 2352:1-11 How to Cite?
AbstractA novel avian-origin influenza A (H7N9) virus emerged in China in 2013 and has caused zoonotic disease in over 1123 persons with an overall mortality around 30%. Amino acid changes at the residues 591, 627 and 701 of polymerase basic protein 2 (PB2) have been found frequently in the human H7N9 isolates but not in viruses isolated from avian species. We have recently identified a cluster of H7N9 viruses in ducks which circulated in China prior to the first recognition of zoonotic disease in 2013. These duck viruses have genetic background distinct from the zoonotic H7N9 lineage. We found that the introduction of PB2 mutation with K at 627 but not K at 591 or N at 701 to the duck H7N9 virus led to increased pathogenicity in mice. We also found that the induction of pro-inflammatory cytokines including TNF-α, IP-10, MCP-1 and MIP-1α were associated with increased severity of infection. We conclude that introduction of the mammalian adaptation mutations into the PB2 gene of duck H7N9 viruses, which are genetically unrelated to the zoonotic H7N9 lineage, can also enhance pathogenicity in mice.
Persistent Identifierhttp://hdl.handle.net/10722/242870
ISSN
2015 Impact Factor: 5.228
2015 SCImago Journal Rankings: 2.073

 

DC FieldValueLanguage
dc.contributor.authorLi, W-
dc.contributor.authorLee, HYH-
dc.contributor.authorLi, RF-
dc.contributor.authorZhu, H-
dc.contributor.authorGuan, Y-
dc.contributor.authorPeiris, JSM-
dc.contributor.authorYang, ZF-
dc.contributor.authorMok, KP-
dc.date.accessioned2017-08-25T02:46:33Z-
dc.date.available2017-08-25T02:46:33Z-
dc.date.issued2017-
dc.identifier.citationScientific Reports, 2017, v. 7 n. 1, p. 2352:1-11-
dc.identifier.issn2045-2322-
dc.identifier.urihttp://hdl.handle.net/10722/242870-
dc.description.abstractA novel avian-origin influenza A (H7N9) virus emerged in China in 2013 and has caused zoonotic disease in over 1123 persons with an overall mortality around 30%. Amino acid changes at the residues 591, 627 and 701 of polymerase basic protein 2 (PB2) have been found frequently in the human H7N9 isolates but not in viruses isolated from avian species. We have recently identified a cluster of H7N9 viruses in ducks which circulated in China prior to the first recognition of zoonotic disease in 2013. These duck viruses have genetic background distinct from the zoonotic H7N9 lineage. We found that the introduction of PB2 mutation with K at 627 but not K at 591 or N at 701 to the duck H7N9 virus led to increased pathogenicity in mice. We also found that the induction of pro-inflammatory cytokines including TNF-α, IP-10, MCP-1 and MIP-1α were associated with increased severity of infection. We conclude that introduction of the mammalian adaptation mutations into the PB2 gene of duck H7N9 viruses, which are genetically unrelated to the zoonotic H7N9 lineage, can also enhance pathogenicity in mice.-
dc.languageeng-
dc.publisherNature Publishing Group: Open Access Journals. The Journal's web site is located at http://www.nature.com/srep/index.html-
dc.relation.ispartofScientific Reports-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleThe PB2 mutation with lysine at 627 enhances the pathogenicity of avian influenza (H7N9) virus which belongs to a non-zoonotic lineage-
dc.typeArticle-
dc.identifier.emailLee, HYH: horlee@hkucc.hku.hk-
dc.identifier.emailZhu, H: zhuhch@hku.hk-
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hk-
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hk-
dc.identifier.emailMok, KP: ch02mkp@hkucc.hku.hk-
dc.identifier.authorityZhu, H=rp01535-
dc.identifier.authorityGuan, Y=rp00397-
dc.identifier.authorityPeiris, JSM=rp00410-
dc.identifier.authorityMok, KP=rp01805-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41598-017-02598-z-
dc.identifier.hkuros274162-
dc.identifier.volume7-
dc.identifier.issue1-
dc.identifier.spage2352:1-
dc.identifier.epage11-
dc.publisher.placeUnited Kingdom-

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