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Twenty amino acids at the C-terminus of PA-X are associated with increased influenza A virus replication and pathogenicity

Gao, Huijie; Sun, Yipeng; Liu, Xiufan; Sun, Honglei; Hu, Jiao; Wang, Jinliang; Lin, Yang; Chang, Kin-Chow; Wang, Yu; Qi, Lu; Pu, Juan; Xiong, Xin; Liu, Jinhua; Seng, Lai-Giea; Kong, Weili; He, Qiming

Authors

Huijie Gao

Yipeng Sun

Xiufan Liu

Honglei Sun

Jiao Hu

Jinliang Wang

Yang Lin

KIN-CHOW CHANG kin-chow.chang@nottingham.ac.uk
Professor of Veterinary Molecular Medicine

Yu Wang

Lu Qi

Juan Pu

Xin Xiong

Jinhua Liu

Lai-Giea Seng

Weili Kong

Qiming He



Abstract

The PA-X protein, arising from ribosomal frameshift during PA translation, was recently discovered in influenza A virus (IAV). The C-terminal domain ‘X’ of PA-X proteins in IAVs can be classified as full-length (61 aa) or truncated (41 aa). In the main, avian influenza viruses express full-length PA-X proteins, whilst 2009 pandemic H1N1 (pH1N1) influenza viruses harbour truncated PA proteins. The truncated form lacks aa 232–252 of the full-length PA-X protein. The significance of PA-X length in virus function remains unclear. To address this issue, we constructed a set of contemporary influenza viruses (pH1N1, avian H5N1 and H9N2) with full and truncated PA-X by reverse genetics to compare their replication and host pathogenicity. All full-length PA-X viruses in human A549 cells conferred 10- to 100-fold increase in viral replication and 5–8 % increase in apoptosis relative to corresponding truncated PA-X viruses. Full-length PA-X viruses were more virulent and caused more severe inflammatory responses in mice. Furthermore, aa 233–252 at the C terminus of PA-X strongly suppressed co-transfected gene expression by ∼50 %, suggesting that these terminal 20 aa could play a role in enhancing viral replication and contribute to virulence.

Citation

Gao, H., Sun, Y., Liu, X., Sun, H., Hu, J., Wang, J., …He, Q. (2015). Twenty amino acids at the C-terminus of PA-X are associated with increased influenza A virus replication and pathogenicity. Journal of General Virology, 96(8), https://doi.org/10.1099/vir.0.000143

Journal Article Type Article
Acceptance Date Apr 10, 2015
Publication Date Aug 1, 2015
Deposit Date Jul 5, 2017
Publicly Available Date Jul 5, 2017
Journal Journal of General Virology
Print ISSN 0022-1317
Electronic ISSN 0022-1317
Publisher Microbiology Society
Peer Reviewed Peer Reviewed
Volume 96
Issue 8
DOI https://doi.org/10.1099/vir.0.000143
Public URL http://eprints.nottingham.ac.uk/id/eprint/43998
Publisher URL https://doi.org/10.1099/vir.0.000143
Copyright Statement Copyright information regarding this work can be found at the following address: http://creativecommons.org/licenses/by/4.0

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Copyright Statement
Copyright information regarding this work can be found at the following address: http://creativecommons.org/licenses/by/4.0





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