Upon entering a cell, alphaherpesvirus capsids are transported toward the minus ends of microtubules and
ultimately deposit virus DNA within the host nucleus. The virus proteins that mediate this centripetal transport are
unknown but are expected to be either viral tegument proteins, which are a group of capsid-associated proteins, or
a surface component of the capsid itself. Starting with derivatives of pseudorabies virus that encode a fluorescent
protein fused to a structural component of the virus, we have made a collection of 12 mutant viruses that lack either
the VP26 capsid protein or an individual tegument protein. Using live-cell fluorescence microscopy, we tracked
individual virus particles in axons following infection of primary sensory neurons. Quantitative analysis of the
VP26-null virus indicates that this protein plays no observable role in capsid transport. Furthermore, viruses lacking
tegument proteins that are nonessential for virus propagation in cell culture were also competent for axonal transport.
These results indicate that a protein essential for viral propagation mediates transport of the capsid to the nucleus.