Genomic characterization of the first human infection caused by avian influenza A (H7N9) virus in Wuhu city
10.3760/cma.j.cn112866-20191121-00184
- VernacularTitle:芜湖市首例人感染A(H7N9)禽流感病毒基因组特征
- Author:
Gongfei WANG
1
;
Yi WANG
;
Jun HE
Author Information
1. 芜湖市疾病预防控制中心 241000
- Keywords:
Low pathogenic avian influenza virus;
A(H7N9);
Genome;
Phylogenetic analysis;
Amino acid mutations
- From:
Chinese Journal of Experimental and Clinical Virology
2020;34(5):551-555
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To analyze the viral genome characteristics of the first human influenza A(H7N9) infection in Wuhu city in 2014.Methods:Samples from a patient diagnosed as positive for the influenza virus A(H7N9) nucleic acid (detected by real-time RT-PCR) were sent to Chinese National Influenza Center for the isolation of strains and genome-wide sequencing. The sequences were submitted to GenBank and Blast was run. Analysis of the homology, key amino acid site mutations and phylogenetic tree of the viral genome were performed with the use of bioinformatics applications, DNAStar Lasergene 7.1 and MEGA7.0.Results:The strain was named A/Wuhu/1/2014(H7N9). Phylogenetic tree analysis of hemagglutinin(HA) showed that the strain belonged to clade W2-4. The cleavage site of HA was PEIPKGR↓G. Compared with the highly pathogenic vaccine strain A/Guangdong/17SF003/2016(H7N9), it lacks 4 amino acid KRTA insertion sequences. T160A, G186V and Q226L mutations occurred in the HA receptor binding site. Five QISNT amino acids (position 69-73) were deleted in the neuraminidase(NA) stalk region. L89V, M535L and E627K mutations were found in PB2. Site mutations occurred in PB1 I368V, PA V100A, K356R and S409N, NS1 P42S and N205S, NS2 T48A, M1 N30D and T215A. The E119V, R152K, H274Y, and R292K mutations were not found in NA, while the S31N mutation appeared in M2.Conclusions:The A/Wuhu/1/2014(H7N9) strain is derived from poultry and originated in the Yangtze River Delta. The virus has an affinity to human receptors and belongs to the low pathogenic avian influenza A (H7N9) viruses (LPAI H7N9). It is sensitive to NA inhibitors and resistant to M2 ion channel inhibitors. The strain has increased virulence in mammals and enhanced adaptability for humans.
