ArticleJournal of virology2011
Herpes simplex virus 1 pUL34 plays a critical role in cell-to-cell spread of virus in addition to its role in virus replication.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Functions of the UL51 protein during the herpesvirus life cycle.Frontiers in microbiology · 2024Review
- The nuclear egress complex of Epstein-Barr virus buds membranes through an oligomerization-driven mechanism.PLoS pathogens · 2022Article
- Features and Functions of the Conserved Herpesvirus Tegument Protein UL11 and Its Binding Partners.Frontiers in microbiology · 2022Review
- Cell Culture Evolution of a Herpes Simplex Virus 1 (HSV-1)/Varicella-Zoster Virus (VZV) UL34/ORF24 Chimeric Virus Reveals Novel Functions for HSV Genes in Capsid Nuclear Egress.Journal of virology · 2021Article
- Article
- Herpes Simplex Virus 1 UL34 Mutants That Affect Membrane Budding Regulation and Nuclear Lamina Disruption.Journal of virology · 2021Article
- HSV-1 Cytoplasmic Envelopment and Egress.International journal of molecular sciences · 2020Review
- Identification of the Capsid Binding Site in the Herpes Simplex Virus 1 Nuclear Egress Complex and Its Role in Viral Primary Envelopment and Replication.Journal of virology · 2019Article
- Roles of the Interhexamer Contact Site for Hexagonal Lattice Formation of the Herpes Simplex Virus 1 Nuclear Egress Complex in Viral Primary Envelopment and Replication.Journal of virology · 2019Article
- Article
- The HSV-1 mechanisms of cell-to-cell spread and fusion are critically dependent on host PTP1B.PLoS pathogens · 2018Article
- What Goes Around, Comes Around - HSV-1 Replication in Monocyte-Derived Dendritic Cells.Frontiers in microbiology · 2017Review
- Extragenic Suppression of a Mutation in Herpes Simplex Virus 1 UL34 That Affects Lamina Disruption and Nuclear Egress.Journal of virology · 2016Article
- A single herpesvirus protein can mediate vesicle formation in the nuclear envelope.The Journal of biological chemistry · 2015Article
- The herpes simplex virus 1 UL51 protein interacts with the UL7 protein and plays a role in its recruitment into the virion.Journal of virology · 2015Article
- Article
- Genome Sequence of the Anterograde-Spread-Defective Herpes Simplex Virus 1 Strain MacIntyre.Genome announcements · 2014Article
- Identification of conserved amino acids in pUL34 which are critical for function of the pseudorabies virus nuclear egress complex.Journal of virology · 2014Article
- The herpes simplex virus 1 UL51 gene product has cell type-specific functions in cell-to-cell spread.Journal of virology · 2014Article
- Mapping of sequences in Pseudorabies virus pUL34 that are required for formation and function of the nuclear egress complex.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Herpes simplex virus (HSV) pUL34 plays a critical role in virus replication by mediating egress of nucleocapsids from the infected cell nucleus. We have identified a mutation in pUL34 (Y68A) that produces a major defect in virus replication and impaired nuclear egress but also profoundly inhibits cell-to-cell spread and trafficking of gE. Virion release to the extracellular medium is not affected by the Y68A mutation, indicating that the mutation specifically inhibits cell-to-cell spread. We isolated extragenic suppressors of the Y68A plaque formation defect and mapped them by a combination of high-throughput Illumina sequencing and PCR-based screening. We found that suppression is highly correlated with a nonsense mutation in the US9 gene, which plays a critical role in cell-to-cell spread of HSV-1 in neurons. The US9 mutation alone is not sufficient to suppress the Y68A spread phenotype, indicating a likely role for multiple viral factors.
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What OpenQuestion holds
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.