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The PB2-K627E mutation attenuates H3N2 swine influenza virus in cultured cells and in mice

tetano

Editor, Senior Moderator
Res Vet Sci. 2017 Nov 11;117:54-56. doi: 10.1016/j.rvsc.2017.11.006. [Epub ahead of print]
[h=1]The PB2-K627E mutation attenuates H3N2 swine influenza virus in cultured cells and in mice.[/h] Gong XQ[SUP]1[/SUP], Ruan BY[SUP]1[/SUP], Liu XM[SUP]1[/SUP], Zhang P[SUP]1[/SUP], Wang XH[SUP]1[/SUP], Wang Q[SUP]1[/SUP], Shan TL[SUP]1[/SUP], Tong W[SUP]1[/SUP], Zhou YJ[SUP]1[/SUP], Li GX[SUP]1[/SUP], Zheng H[SUP]1[/SUP], Tong GZ[SUP]2[/SUP], Yu H[SUP]3[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] PB2-627K is an important amino acid that determines the virulence of some influenza A viruses. However, it has not been experimentally investigated in the H3N2 swine influenza virus. To explore the potential role of PB2-K627E substitution in H3N2 swine influenza virus, the growth properties and pathogenicity between H3N2 swine influenza virus and its PB2-K627E mutant were compared. For the first time, our results showed that PB2-K627E mutation attenuates H3N2 swine influenza virus in mammalian cells and in mice, suggesting that PB2-627K is required for viral replication and pathogenicity of H3N2 swine influenza virus.


[h=4]KEYWORDS:[/h] PB2?627; Pathogenicity; Swine influenza virus; Virulence

PMID: 29175013 DOI: 10.1016/j.rvsc.2017.11.006
 
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