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Volume 24, Number 4—April 2018
Dispatch

Enhanced Replication of Highly Pathogenic Influenza A(H7N9) Virus in Humans

Seiya Yamayoshi1, Maki Kiso, Atsuhiro Yasuhara, Mutsumi Ito, Yuelong Shu, and Yoshihiro Kawaoka1Comments to Author 
Author affiliations: University of Tokyo, Tokyo, Japan (S. Yamayoshi, M. Kiso, A. Yasuhara, M. Ito, Y. Kawaoka); Sun Yat-Sen University, Shenzhen, China (Y. Shu); Chinese Centers for Disease Control and Prevention, Beijing, China (Y. Shu); University of Wisconsin–Madison, Madison, Wisconsin, USA, and Japan Science and Technology Agency, Saitama, Japan (Y. Kawaoka)

Main Article

Figure 1

Viral polymerase activity of wild-type, PB2 mutant, and PA mutant polymerase complexes. A) Viral polymerase activities of highly pathogenic influenza A(H7N9) virus GD replication complexes harboring amino acid substitutions in PB2 (A), PA (B), or PB2 and PA (C) in human A549 and chicken DF-1 cells. The data shown are relative polymerase activities ± SD (n = 3). The polymerase activity of GD wild-type was set to 100%. **p<0.01, according to a 1-way analysis of variance followed by a Dunnett te

Figure 1. Viral polymerase activity of wild-type, PB2 mutant, and PA mutant polymerase complexes. A) Viral polymerase activities of highly pathogenic influenza A(H7N9) virus GD replication complexes harboring amino acid substitutions in PB2 (A), PA (B), or PB2 and PA (C) in human A549 and chicken DF-1 cells. The data shown are relative polymerase activities ± SD (n = 3). The polymerase activity of GD wild-type was set to 100%. **p<0.01, according to a 1-way analysis of variance followed by a Dunnett test. Error bars indicate SD. AN, A/Anhui/1/2013(H7N9); GD, A/Guangdong/17SF003/2016; PA, polymerase acidic; PB, polymerase basic.

Main Article

1These senior authors contributed equally to this article.

Page created: March 19, 2018
Page updated: March 19, 2018
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