期刊
JOURNAL OF VIROLOGY
卷 86, 期 9, 页码 5366-5370出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.06722-11
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资金
- NIH (Center for Research on Influenza Pathogenesis [CRIP])
- NIH (NIAID CEIRS) [HHSN266200700010C]
- NIH (NIAID) [RO1AI046954]
- National Institutes of Health-National Cancer Institute (NIH-NCI) [5R24 CA095823-04]
- NSF [DBI-9724504]
- NIH [1 S10 RR0 9145-01]
- Medical Research Council [G0801822] Funding Source: researchfish
- MRC [G0801822] Funding Source: UKRI
We generated influenza A viruses expressing mutant NS1 proteins unable to activate phosphoinositide 3-kinase (PI3K) in two mouse-lethal strains. The recombinant A/Puerto Rico/8/34 (rPR8) mutant virus strain was attenuated and caused reduced morbidity/mortality. For the recombinant A/WSN/33 (rWSN) virus strain, the inability to stimulate PI3K had minimal impact on replication or morbidity/mortality. Cell-based assays revealed subtly distinct intracellular sites of NS1 localization and PI3K activation between the strains. We hypothesize that specific spatially regulated NS1-activated PI3K signaling, rather than simply the total level of active PI3K, is important for virus replication and virulence.
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