Abstract
Pseudorabies virus (PRV), an alphaherpesvirus, is sorted and transported in axons in the anterograde direction by the kinesin-3 motor KIF1A. Huang et al. (e01934-19) showed that PRV neuronal infection disrupts KIF1A synthesis and accelerates proteasomal degradation of intrinsically unstable KIF1A proteins in axons, leading to depletion of the motor late in infection. The viral anterograde sorting complex US9/gE/gI mediates the accelerated KIF1A degradation. These findings suggest that following a reactivation episode in peripheral nervous system (PNS) neurons, PRV progeny have a limited time window in which to travel back to the mucosal surface for further host-to-host spread.
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