The pseudorabies virus protein, pUL56, enhances virus dissemination and virulence but is dispensable for axonal transport

Gina R. Daniel; Patricia J. Sollars; Gary E. Pickard; Gregory A. Smith

doi:10.1016/j.virol.2015.11.014

The pseudorabies virus protein, pUL56, enhances virus dissemination and virulence but is dispensable for axonal transport

Gina R. Daniel, Patricia J. Sollars, Gary E. Pickard, Gregory A. Smith^*

^*Corresponding author for this work

Microbiology-Immunology

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

Neurotropic herpesviruses exit the peripheral nervous system and return to exposed body surfaces following reactivation from latency. The pUS9 protein is a critical viral effector of the anterograde axonal transport that underlies this process. We recently reported that while pUS9 increases the frequency of sorting of newly assembled pseudorabies virus particles to axons from the neural soma during egress, subsequent axonal transport of individual virus particles occurs with wild-type kinetics in the absence of the protein. Here, we examine the role of a related pseudorabies virus protein, pUL56, during neuronal infection. The findings indicate that pUL56 is a virulence factor that supports virus dissemination in vivo, yet along with pUS9, is dispensable for axonal transport.

Original language	English (US)
Pages (from-to)	179-186
Number of pages	8
Journal	Virology
Volume	488
DOIs	https://doi.org/10.1016/j.virol.2015.11.014
State	Published - Jan 15 2016

Funding

This work was supported by NIH Grant R01 AI056346 to G.A.S. and R01 NS077003 to G.E.P. and P.J.S. G.R.D was supported by the training program in the Cellular and Molecular Basis of Disease from the National Institutes of Health ( T32 GM08061 ). We thank Anne Fischer and Stephanie Totten for excellent technical assistance, and Jenifer Klabis for help with figure illustrations.

Keywords

Herpesvirus
Nervous system
PRV
UL56
US9
Virulence

ASJC Scopus subject areas

Virology

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10.1016/j.virol.2015.11.014

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title = "The pseudorabies virus protein, pUL56, enhances virus dissemination and virulence but is dispensable for axonal transport",

abstract = "Neurotropic herpesviruses exit the peripheral nervous system and return to exposed body surfaces following reactivation from latency. The pUS9 protein is a critical viral effector of the anterograde axonal transport that underlies this process. We recently reported that while pUS9 increases the frequency of sorting of newly assembled pseudorabies virus particles to axons from the neural soma during egress, subsequent axonal transport of individual virus particles occurs with wild-type kinetics in the absence of the protein. Here, we examine the role of a related pseudorabies virus protein, pUL56, during neuronal infection. The findings indicate that pUL56 is a virulence factor that supports virus dissemination in vivo, yet along with pUS9, is dispensable for axonal transport.",

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AU - Smith, Gregory A.

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AB - Neurotropic herpesviruses exit the peripheral nervous system and return to exposed body surfaces following reactivation from latency. The pUS9 protein is a critical viral effector of the anterograde axonal transport that underlies this process. We recently reported that while pUS9 increases the frequency of sorting of newly assembled pseudorabies virus particles to axons from the neural soma during egress, subsequent axonal transport of individual virus particles occurs with wild-type kinetics in the absence of the protein. Here, we examine the role of a related pseudorabies virus protein, pUL56, during neuronal infection. The findings indicate that pUL56 is a virulence factor that supports virus dissemination in vivo, yet along with pUS9, is dispensable for axonal transport.

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The pseudorabies virus protein, pUL56, enhances virus dissemination and virulence but is dispensable for axonal transport

Abstract

Funding

Keywords

ASJC Scopus subject areas

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