Full-Genome Analysis of Influenza A(H7N9) Virus from Shanghai, China, 2014

[tetano]

Genome Announc. 2014 Jun 19;2(3). pii: e00578-14. doi: 10.1128/genomeA.00578-14.
Full-Genome Analysis of Influenza A(H7N9) Virus from Shanghai, China, 2014.
Zhang W1, He Y2, Xu L1, Dai F1, Mei Z2, Qian L2, Xie D2, Shen Y2, Gu Y2, Zhang Z1, Yuan Z, Jie Z3, Hu Y4.
Author information
Abstract

We analyzed the complete genome sequence of the A/Shanghai/01/2014 (H7N9) strain, which will provide a better understanding of the evolution of influenza A(H7N9) virus.

Copyright ? 2014 Zhang et al.

PMID:
24948761
[PubMed]
PMCID:
PMC4064026

Free PMC Article

http://www.ncbi.nlm.nih.gov/pubmed/24948761

 

[sharon sanders]

Re: Full-Genome Analysis of Influenza A(H7N9) Virus from Shanghai, China, 2014

Full-Genome Analysis of Influenza A(H7N9) Virus from Shanghai, China, 2014
Wanju Zhanga, Yanchao Heb, Lei Xua, Fahui Daia, Zhoufang Meib, Ling Qianb, Desheng Xieb, Ying Shenb, Yong Gub, Zhiyong Zhanga, Zhenghong Yuana,c, Zhijun Jieb, Yunwen Hua,c
+ Author Affiliations

aPathogen Diagnosis and Biosafety Department, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
bDepartment of Respiratory Medicine, Fifth People’s Hospital of Shanghai, Fudan University, Shanghai, China
cKey Laboratory of Medical Molecular Virology, School of Basic Medical Science, Shanghai Medical College of Fudan University, Shanghai, China

Next Section
ABSTRACT

We analyzed the complete genome sequence of the A/Shanghai/01/2014 (H7N9) strain, which will provide a better understanding of the evolution of influenza A(H7N9) virus.

Previous Section
Next Section
GENOME ANNOUNCEMENT

Influenza A virus (IAV), which is a member of the genus Influenzavirus, family Orthomyxoviridae, contains 8 single-stranded negative-sense RNA (-ssRNA) segments that encode 12 proteins. Recently, a novel avian-origin influenza A(H7N9) virus has caused >410 cases of infection in China, including 60 deaths from March 2013 to 8 April 2014 (1). Influenza A(H7N9) cases worldwide were first found in the Minhang district of Shanghai in 2013 (2). No more cases were discovered in this area after May 2013, until the first Shanghai H7N9 case of 2014 reemerged in the same area in January. The patient, an 86-year-old man, was admitted to the Fifth People’s Hospital of Shanghai with a 4-day history of fever (up to 40°C) with cough on 30 December 2013. The throat swabs and sputum samples were collected on the day of admission and day 4 after admission. Viral RNA extracted from the samples was subjected to real-time reverse transcription-PCR (RT-PCR) for detecting influenza type A and subtype A(H7N9) according to the protocol provided by the Chinese CDC (3, 4). Viral RNA extracted from the supernatant of the sputa was subjected to amplify each of the viral gene segments using the One-Step RT-PCR kit (Qiagen, Inc.) using a set of gene-specific primers. The PCR products were directly sequenced with an ABI 3730XL automatic DNA analyzer using the ABI Prism BigDye Terminator cycle sequencing kit 3.1.

All gene segments of the A/Shanghai/01/2014 (H7N9) virus were compared with those of the vaccine component strain A/Anhui1/1/2013 and those of the currently circulating strains. The complete coding region of A/Shanghai/01/2014 (H7N9) is 13,090 nucleotides long. Segments 1 to 8 are 2,280, 2,274, 2,151, 1,683, 1,497, 1,398, 969, and 838 nucleotides (nt), respectively. The strain has an amantadine resistance mutation (S31N substitution) in the viral M2 protein and no oseltamivir resistance mutation (R292K substitution) in the viral neuraminidase (NA) protein (5). The mutation encoding E627K in the polymerase basic 2 (PB2) protein, which confers high virulence to avian influenza in mammalian hosts (6), was not found.

The similarities of the PB1, polymerase acidic (PA), hemagglutinin (HA), nucleoprotein (NP), NA, matrix (M), and nonstructural (NS) genes between the sequence of A/Shanghai/01/2014 (H7N9) and the consensus sequence of 2013 strains (n = 34) were all >99.9%, while the similarity of the PB2 gene was only 96.8%. Phylogenetic analysis indicated that the PB2 gene of the A/Shanghai/01/2014 (H7N9) virus was not clustered with those of the human H7N9 strains in 2013 but clustered with those of A/Chicken/Wenzhou/598/2013 (H9N2) and A/Chicken/Wenzhou/642/2013 (H9N2). The similarities of the PB2 nucleic acid sequences between the A/Shanghai/01/2014 (H7N9) and A/Chicken/Wenzhou/598/2013 (H9N2) strains were as high as 99.6%, which suggests that the origin of the PB2 gene fragment in the A/Shanghai/01/2014 (H7N9) virus strain was different from those of human strains in 2013. The sequence information reported here will facilitate further investigations of the evolution of human infected avian-origin H7N9 influenza virus.

Nucleotide sequence accession numbers.The complete genome sequence of the A/Shanghai/01/2014 (H7N9) strain has been deposited and updated in GenBank under the accession no. KJ411975 to KJ411982.

Previous Section
Next Section
ACKNOWLEDGMENTS

This research was supported by the National Megaprojects of China for Infectious Disease (2012ZX10004211 and 2014ZX10004002-005), National Natural Science Foundation of China (81341004, 81102283, and 81370131), Outstanding Academic Leader of Health System in Shanghai (XBR2013078), Ministry of Science and Technology (KJYJ-2013-01-01), and Shanghai Municipal Health and Family Planning Commission (2013QLG002).

Previous Section
Next Section
FOOTNOTES

Address correspondence to Zhijun Jie, jiezjlxh@gmail.com, or Yunwen Hu, ywhu0117@126.com.
W. Zhang, Y. He, and L. Xu contributed equally to this work.
Citation Zhang W, He Y, Xu L, Dai F, Mei Z, Qian L, Xie D, Shen Y, Gu Y, Zhang Z, Yuan Z, Jie H, Hu Y. 2014. Full-genome analysis of influenza A(H7N9) virus from Shanghai, China, 2014. Genome Announc. 2(3):e00578-14. doi:10.1128/genomeA.00578-14.
Received 21 May 2014. Accepted 6 June 2014. Published 19 June 2014.
Copyright © 2014 Zhang et al.
This is an open-access article distributed under the terms of the Creative Commons Attribution 3.0 Unported license.

http://genomea.asm.org/content/2/3/e00578-14.full

 

[sharon sanders]

Genetic tuning of the novel avian influenza a(h7n9) virus during interspecies transmission, china, 2013

Genetic tuning of the novel avian influenza a(h7n9) virus during interspecies transmission, china, 2013

Eurosurveillance, Volume 19, Issue 25, 26 June 2014
Research articles
GENETIC TUNING OF THE NOVEL AVIAN INFLUENZA A(H7N9) VIRUS DURING INTERSPECIES TRANSMISSION, CHINA, 2013
D Wang1,2, L Yang1,2, R Gao1, X Zhang3, Y Tan4, A Wu5, W Zhu1, J Zhou1, S Zou1, Xiyan Li1, Y Sun6, Y Zhang7, Y Liu8, T Liu9, Y Xiong10, J Xu11, L Chen12, Y Weng13, X Qi14, J Guo1, Xiaodan Li1, J Dong1, W Huang1, Y Zhang1, L Dong1, X Zhao1, L Liu1, J Lu1, Y Lan1, H Wei1, L Xin1, Y Chen1, C Xu1, T Chen1, Y Zhu1, T Jiang5, Z Feng15, W Yang15, Y Wang15, H Zhu16, Y Guan16, G F Gao15, D Li1, J Han1, S Wang1, G Wu1, Y Shu ()1
National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Key Laboratory for Medical Virology, National Health and Family Planning Commission, Beijing, China
These authors contributed equally to this work
Shanghai Municipal Disease Control and Prevention, Shanghai, China
Guangxi Center for Disease Control and Prevention, Nanning, China
Institutes of Biophysics, Chinese Academy of Sciences, Beijing, China
Anhui Provincial Disease Control and Prevention, Hefei, China
Zhejiang Provincial Disease Control and Prevention, Hangzhou, China
Hunan Provincial Disease Control and Prevention, Changsha, China
Shandong Provincial Disease Control and Prevention, Jinan, China
Jiangxi Provincial Disease Control and Prevention, Nanchang, China
Henan Provincial Disease Control and Prevention, Zhengzhou, China
Beijing Municipal Disease Control and Prevention, Beijing, China
Fujian Provincial Disease Control and Prevention, Fuzhou, China
Jiangsu Provincial Disease Control and Prevention, Nanjing, China
Chinese Center for Disease Control and Prevention, Beijing, China
The University of Hong Kong, Hong Kong SAR, China
Citation style for this article: Wang D, Yang L, Gao R, Zhang X, Tan Y, Wu A, Zhu W, Zhou J, Zou S, Li X, Sun Y, Zhang Y, Liu Y, Liu T, Xiong Y, Xu J, Chen L, Weng Y, Qi X, Guo J, Li X, Dong J, Huang W, Zhang Y, Dong L, Zhao X, Liu L, Lu J, Lan Y, Wei H, Xin L, Chen Y, Xu C, Chen T, Zhu Y, Jiang T, Feng Z, Yang W, Wang Y, Zhu H, Guan Y, Gao GF, Li D, Han J, Wang S, Wu G, Shu Y. Genetic tuning of the novel avian influenza A(H7N9) virus during interspecies transmission, China, 2013 . Euro Surveill. 2014;19(25)ii=20836. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20836

Date of submission: 28 July 2013
A 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.

http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20836