File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Genetic tuning of the novel avian influenza A(H7N9) virus during interspecies transmission, China, 2013

TitleGenetic tuning of the novel avian influenza A(H7N9) virus during interspecies transmission, China, 2013
Authors
Issue Date2014
PublisherEuropean Centre for Disease Prevention and Control. The Journal's web site is located at http://www.eurosurveillance.org/Public/AboutUs/AboutUs.aspx
Citation
Eurosurveillance, 2014, v. 19 n. 25, article no. 20836 How to Cite?
AbstractA novel avian influenza A(H7N9) virus causing human infection emerged in February 2013 in China. To elucidate the mechanism of interspecies transmission, we compared the signature amino acids of avian influenza A(H7N9) viruses from human and non-human hosts and analysed the reassortants of 146 influenza A(H7N9) viruses with full genome sequences. We propose a genetic tuning procedure with continuous amino acid substitutions and reassorting that mediates host adaptation and interspecies transmission. When the early influenza A(H7N9) virus, containing ancestor haemagglutinin (HA) and neuraminidase (NA) genes similar to A/Shanghai/05 virus, circulated in waterfowl and transmitted to terrestrial poultry, it acquired an NA stalk deletion at amino acid positions 69 to 73. Then, receptor binding preference was tuned to increase the affinity to human-like receptors through HA G186V and Q226L mutations in terrestrial poultry. Additional mammalian adaptations such as PB2 E627K were selected in humans. The continual reassortation between H7N9 and H9N2 viruses resulted in multiple genotypes for further host adaptation. When we analysed a potential association of mutations and reassortants with clinical outcome, only the PB2 E627K mutation slightly increased the case fatality rate. Genetic tuning may create opportunities for further adaptation of influenza A(H7N9) and its potential to cause a pandemic.
Persistent Identifierhttp://hdl.handle.net/10722/202036
ISSN
2023 Impact Factor: 9.9
2023 SCImago Journal Rankings: 2.881

 

DC FieldValueLanguage
dc.contributor.authorWang, Den_US
dc.contributor.authorYang, Len_US
dc.contributor.authorGao, Ren_US
dc.contributor.authorZhang, Xen_US
dc.contributor.authorTan, Yen_US
dc.contributor.authorWu, Aen_US
dc.contributor.authorZhu, Wen_US
dc.contributor.authorZhou, Jen_US
dc.contributor.authorZou, Sen_US
dc.contributor.authorLi, Xen_US
dc.contributor.authorSun, Yen_US
dc.contributor.authorZhang, Yen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorLiu, Ten_US
dc.contributor.authorXiong, Yen_US
dc.contributor.authorXu, Jen_US
dc.contributor.authorChen, Len_US
dc.contributor.authorWeng, Yen_US
dc.contributor.authorQi, Xen_US
dc.contributor.authorGuo, Jen_US
dc.contributor.authorLi, Xen_US
dc.contributor.authorDong, Jen_US
dc.contributor.authorHuang, Wen_US
dc.contributor.authorZhang, Yen_US
dc.contributor.authorDong, Len_US
dc.contributor.authorZhao, Xen_US
dc.contributor.authorLiu, Len_US
dc.contributor.authorLu, Jen_US
dc.contributor.authorLan, Yen_US
dc.contributor.authorWei, Hen_US
dc.contributor.authorXin, Len_US
dc.contributor.authorChen, Yen_US
dc.contributor.authorXu, Cen_US
dc.contributor.authorChen, Ten_US
dc.contributor.authorZhu, Yen_US
dc.contributor.authorJiang, Ten_US
dc.contributor.authorFeng, Zen_US
dc.contributor.authorYang, Wen_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorZhu, Hen_US
dc.contributor.authorGuan, Yen_US
dc.contributor.authorGao, Gen_US
dc.contributor.authorLi, Den_US
dc.contributor.authorHan, Jen_US
dc.contributor.authorWang, Sen_US
dc.contributor.authorWu, Gen_US
dc.contributor.authorShu, Yen_US
dc.date.accessioned2014-08-21T07:59:35Z-
dc.date.available2014-08-21T07:59:35Z-
dc.date.issued2014en_US
dc.identifier.citationEurosurveillance, 2014, v. 19 n. 25, article no. 20836en_US
dc.identifier.issn1025-496X-
dc.identifier.urihttp://hdl.handle.net/10722/202036-
dc.description.abstractA novel avian influenza A(H7N9) virus causing human infection emerged in February 2013 in China. To elucidate the mechanism of interspecies transmission, we compared the signature amino acids of avian influenza A(H7N9) viruses from human and non-human hosts and analysed the reassortants of 146 influenza A(H7N9) viruses with full genome sequences. We propose a genetic tuning procedure with continuous amino acid substitutions and reassorting that mediates host adaptation and interspecies transmission. When the early influenza A(H7N9) virus, containing ancestor haemagglutinin (HA) and neuraminidase (NA) genes similar to A/Shanghai/05 virus, circulated in waterfowl and transmitted to terrestrial poultry, it acquired an NA stalk deletion at amino acid positions 69 to 73. Then, receptor binding preference was tuned to increase the affinity to human-like receptors through HA G186V and Q226L mutations in terrestrial poultry. Additional mammalian adaptations such as PB2 E627K were selected in humans. The continual reassortation between H7N9 and H9N2 viruses resulted in multiple genotypes for further host adaptation. When we analysed a potential association of mutations and reassortants with clinical outcome, only the PB2 E627K mutation slightly increased the case fatality rate. Genetic tuning may create opportunities for further adaptation of influenza A(H7N9) and its potential to cause a pandemic.-
dc.languageengen_US
dc.publisherEuropean Centre for Disease Prevention and Control. The Journal's web site is located at http://www.eurosurveillance.org/Public/AboutUs/AboutUs.aspx-
dc.relation.ispartofEurosurveillanceen_US
dc.titleGenetic tuning of the novel avian influenza A(H7N9) virus during interspecies transmission, China, 2013en_US
dc.typeArticleen_US
dc.identifier.emailZhu, H: zhuhch@hku.hken_US
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_US
dc.identifier.authorityZhu, H=rp01535en_US
dc.identifier.authorityGuan, Y=rp00397en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.2807/1560-7917.ES2014.19.25.20836-
dc.identifier.pmid24993557-
dc.identifier.scopuseid_2-s2.0-84921899121-
dc.identifier.hkuros232587en_US
dc.identifier.volume19en_US
dc.identifier.issnl1025-496X-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats