RT info:eu-repo/semantics/article
T1 Strain-Specific Contribution of NS1-Activated Phosphoinositide 3-Kinase Signaling to Influenza A Virus Replication and Virulence
A1 Ayllón Barasoain, Juan
A1 Hale, Benjamin G.
A1 García Sastre, Adolfo
K1 Medicina
K1 Medicine
K1 Salud
K1 Health
K1 Microbiología
K1 Microbiology
K1 Enfermedades infecciosas
K1 Communicable diseases
AB We generated influenza A viruses expressing mutant NS1 proteins unable to activate phosphoinositide 3-kinase (PI3K) in twomouse-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 onreplication or morbidity/mortality. Cell-based assays revealed subtly distinct intracellular sites of NS1 localization and PI3Kactivation between the strains. We hypothesize that specific spatially regulated NS1-activated PI3K signaling, rather than simplythe total level of active PI3K, is important for virus replication and virulence.
PB American Society for Microbiology
SN 0022-538X
YR 2012
FD 2012-05
LK http://hdl.handle.net/10259/9525
UL http://hdl.handle.net/10259/9525
LA eng
NO This work was supported by NIH funding to A.G.-S. (Center for Research on Influenza Pathogenesis [CRIP], NIAID CEIRS contract HHSN266200700010C, and NIAID grant RO1AI046954). Confocal laser scanning microscopy was performed at the MSSM-Microscopy Shared Resource Facility, which is supported with funding from a National Institutes of Health-National Cancer Institute (NIH-NCI) shared resources grant (5R24 CA095823-04), an NSF Major Research Instrumentation grant (DBI-9724504), and an NIH shared instrumentation grant (1 S10 RR0 9145-01).
DS Repositorio Institucional de la Universidad de Burgos
RD 23-nov-2024