2026-06-17T18:23:26Zhttps://riubu.ubu.es/oai/request

oai:riubu.ubu.es:10259/95252024-09-05T00:05:22Zcom_10259_4862com_10259_5086com_10259_2604col_10259_4863

Ayllón Barasoain, Juan Hale, Benjamin G. García Sastre, Adolfo 2024-09-04T07:54:51Z 2024-09-04T07:54:51Z 2012-05 0022-538X http://hdl.handle.net/10259/9525 10.1128/jvi.06722-11 1098-5514 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. eng info:eu-repo/semantics/openAccess Strain-Specific Contribution of NS1-Activated Phosphoinositide 3-Kinase Signaling to Influenza A Virus Replication and Virulence info:eu-repo/semantics/article