Key result
Mutations in the NS2 (NEP) NES motif that maintain hydrophobicity allow CRM1-mediated nuclear export of vRNPs, though some mutants exhibit delayed export and limited viral growth.
Population
Influenza A virus NS2 (NEP) mutants, cell culture, and mice models
Comparison
Random mutations introduced by degenerative… vs Wild-type Influenza A virus
Design
Preclinical
Authors
Loading...
Supports NS2 NES targeting for attenuation in models; leaves open translation to safe human live vaccines.
The NES motif of the influenza A virus NS2 (NEP) protein requires conserved hydrophobicity for CRM1-mediated nuclear export, and mutations in this region can attenuate viral growth, offering a potential target for live vaccine development.
Iwatsuki‐Horimoto et al. (2004) studied Influenza A virus infection. Mutations in the NS2 (NEP) NES motif vs. Wild-type virus was evaluated on Nuclear export of vRNPs and viral growth. Mutations in the NS2 (NEP) NES motif that maintain hydrophobicity allow CRM1-mediated nuclear export of vRNPs, though some mutants exhibit delayed export and limited viral growth.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: