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Heterologous SH3-p85β inhibits influenza A virus replication

Authors: Chi Zhang; Xiaoxuan Chen; Wei-Zhong Li; Xiang-xing Zeng; Yun Su; Yanxuan Xu; Gefei Wang; +3 Authors

Heterologous SH3-p85β inhibits influenza A virus replication

Abstract

Abstract Phosphatidylinositol 3-kinase (PI3K)/Akt signalling pathway can support the replication of influenza A virus through binding of viral NS1 protein to the Src homology 3 (SH3) domain of p85β regulatory subunit of PI3K. Here we investigated the effect of heterologously overexpressed SH3 on the replication of different influenza A virus subtypes/strains, and on the phosphorylation of Akt in the virus-infected cells. We found that heterologous SH3 reduced replication of influenza A viruses at varying degrees in a subtype/strain-dependent manner and SH3 overexpression reduced the induction of the phosphorylation of Akt in the cells infected with PR8(H1N1) and ST364(H3N2), but not with ST1233(H1N1), Ph2246(H9N2), and Qa199(H9N2). Our results suggest that interference with the NS1-p85β interaction by heterologous SH3 can be served as a useful antiviral strategy against influenza A virus infection.

Related Organizations
Keywords

Research, Down-Regulation, Infectious and parasitic diseases, RC109-216, Viral Nonstructural Proteins, Virus Replication, Cell Line, src Homology Domains, Phosphatidylinositol 3-Kinases, Protein Subunits, Infectious Diseases, Dogs, Influenza A virus, Virology, Influenza, Human, Animals, Humans, Phosphorylation, Proto-Oncogene Proteins c-akt, Protein Binding

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    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
9
Average
Average
Average
Green
gold