Pseudorabies virus pUL40 drives inflammatory signaling through competitive hijacking of EphA2 from the Akt–EphA2 interaction
These findings reveal a proviral strategy whereby PRV UL40 hijacks EphA2 to counteract an intrinsic Akt-dependent inhibitory pathway, and EphA2 S897 represents a potential therapeutic target for mitigating alphaherpesvirus immunopathology.