FIG 8.

PRV infection induces the accelerated loss of KIF1A protein through two separate mechanisms. (A) In uninfected cells, KIF1A protein is inherently prone to be degraded by the proteasome. The steady-state concentration of KIF1A protein is achieved through rapid protein synthesis and proteasomal degradation. (B) PRV infection induces KIF1A mRNA degradation and reduced protein synthesis, while the existing KIF1A proteins undergo default proteasomal degradation. Furthermore, the proteasomal degradation of the existing KIF1A proteins is accelerated by the PRV gE/gI/US9 complex in the late phase of infection. Images were created with BioRender.