ArticleVirology2016
The pseudorabies virus protein, pUL56, enhances virus dissemination and virulence but is dispensable for axonal transport.
Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- Comparative Phenotypic Characterization of Five CRISPR/Cas9-Generated Gene-Disrupted Mutants of Pseudorabies Virus JM Strain.Veterinary sciences · 2026Article
- Construction of pseudorabies virus variant attenuated vaccine: codon deoptimization ofFrontiers in microbiology · 2023Article
- Motor Skills: Recruitment of Kinesins, Myosins and Dynein during Assembly and Egress of Alphaherpesviruses.Viruses · 2021Review
- Engagement of Neurotropic Viruses in Fast Axonal Transport: Mechanisms, Potential Role of Host Kinases and Implications for Neuronal Dysfunction.Frontiers in cellular neuroscience · 2021Article
- Host BAG3 Is Degraded by Pseudorabies Virus pUL56 C-TerminalInternational journal of molecular sciences · 2020Article
- A GFP-tagged version of the pseudorabies virus protein UL56 localizes to the Golgi and trans-Golgi network through a predicted C-terminal leucine-rich helix in transfected cells.Virology journal · 2019Article
- Review
- Inner tegument proteins of Herpes Simplex Virus are sufficient for intracellular capsid motility in neurons but not for axonal targeting.PLoS pathogens · 2017Article
- Multi-Platform Sequencing Approach Reveals a Novel Transcriptome Profile in Pseudorabies Virus.Frontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.