ArticleViruses2015
Herpes simplex virus 1 Us3 deletion mutant is infective despite impaired capsid translocation to the cytoplasm.
Article in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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
15 citing papers in PubMed, 17 citations in OpenAlex.
- GRWD1 enhances HSV-1 replication by facilitating nuclear egress.Microbiology spectrum · 2026Article
- Article
- Molecular plasticity of herpesvirus nuclear egress analysed in situ.Nature microbiology · 2024Article
- Herpes Simplex Virus: The Hostile Guest That Takes Over Your Home.Frontiers in microbiology · 2020Review
- Nuclear envelope impairment is facilitated by the herpes simplex virus 1 Us3 kinase.F1000Research · 2019Article
- The herpes simplex virus 1 Us3 kinase is involved in assembly of membranes needed for viral envelopment and in distribution of glycoprotein K.F1000Research · 2019Article
- Experimental Dissection of the Lytic Replication Cycles of Herpes Simplex VirusesFrontiers in microbiology · 2018Review
- The suppression of apoptosis by α-herpesvirus.Cell death & disease · 2017Review
- Visualization of DNA G-quadruplexes in herpes simplex virus 1-infected cells.Nucleic acids research · 2016Article
- The mutated tegument protein UL7 attenuates the virulence of herpes simplex virus 1 by reducing the modulation of α-4 gene transcription.Virology journal · 2016Article
- HSV-1 tegument protein and the development of its genome editing technology.Virology journal · 2016Review
- Article
- Article
- The UL13 and US3 Protein Kinases of Herpes Simplex Virus 1 Cooperate to Promote the Assembly and Release of Mature, Infectious Virions.PloS one · 2015Article
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus 1 (HSV-1) capsids are assembled in the nucleus bud at the inner nuclear membrane into the perinuclear space, acquiring envelope and tegument. In theory, these virions are de-enveloped by fusion of the envelope with the outer nuclear membrane and re-enveloped by Golgi membranes to become infective. Us3 enables the nucleus to cytoplasm capsid translocation. Nevertheless, Us3 is not essential for the production of infective progeny viruses. Determination of phenotype distribution by quantitative electron microscopy, and calculation per mean nuclear or cell volume revealed the following: (i) The number of R7041(∆US3) capsids budding at the inner nuclear membrane was significantly higher than that of wild type HSV-1; (ii) The mean number of R7041(∆US3) virions per mean cell volume was 2726, that of HSV-1 virions 1460 by 24 h post inoculation; (iii) 98% of R7041(∆US3) virions were in the perinuclear space; (iv) The number of R7041(∆US3) capsids in the cytoplasm, including those budding at Golgi membranes, was significantly reduced. Cell associated R7041(∆US3) yields were 2.37×10(8) and HSV-1 yields 1.57×10(8) PFU/mL by 24 h post inoculation. We thus conclude that R7041(∆US3) virions, which acquire envelope and tegument by budding at the inner nuclear membrane into the perinuclear space, are infective.
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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.