期刊
VIROLOGY
卷 396, 期 1, 页码 94-105出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2009.10.004
关键词
Influenza A virus; Reverse genetics; NS1; Apoptosis; PI3K
类别
资金
- Medical Research Council, UK
- Interdisciplinary Centre for Human and Avian Influenza Research (ICHAIR)
- Scottish Funding Council, UK
- BBSRC
- Medical Research Council [G0601126] Funding Source: researchfish
- MRC [G0601126] Funding Source: UKRI
A panel of influenza A viruses encoding mutant NS1 proteins was created in which a number of NS1 functions, including interactions with dsRNA, PI3K, CPSF30 and PKR, were inhibited. Surprisingly, given previous reports that NS1 activates PI3K to prevent apoptosis, the mutant viruses rUd-Y89F and rUd-P164/7A that fail to activate PI3K did not induce any more apoptosis than wild-type virus in MRC-5 and A549 cells, even though these cells are highly sensitive to inducers of apoptosis. Induction of cell death by the apoptogenic rUd-184-8(P) virus could not be prevented by serum-mediated activation of PI3K/Akt. Neither infection of MRC-5 or A549 cells with wild-type virus nor constitutive expression of NS1 prevented cell death caused by apoptosis inducers, suggesting that NS1 is not directly anti-apoptotic. Our data suggest that the loss of a functionally intact NS1 protein promotes apoptosis, but this is not due to an inability to activate PI3K. (C) 2009 Elsevier Inc. All rights reserved.
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