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Grail is a well-characterized mediator of metabolic disease, tumour progression, and immune response. However, its role in influenza A virus (IAV) infection remains poorly understood. In this study, we demonstrated that  Grail  knockdown potentiates IAV infection, whereas Grail overexpression blocks IAV replication. The intranasal administration of IAV to  Grail  KO mice led to a lower survival rate than in similarly infected wild-type mice. Additionally, IAV-infected  Grail  KO mice had higher viral titres, greater immune cell infiltration, and increased expression of inflammatory cytokines in the lungs. Mechanistically, we showed that Grail interacts with viral nucleoprotein (NP), targeting it for degradation and inhibiting IAV replication. NP expression was increased in  Grail  knockdown cells and reduced in cells overexpressing  Grail . Collectively, our results demonstrate that Grail acts as a negative regulator of IAV infection and replication by degrading viral NP. These data increase our understanding of the host antiviral response to infection with IAV.

Grail attenuates influenza A virus infection and pathogenesis by inhibiting viral nucleoprotein