ArticleJournal of virology2004
Redistribution of cellular and herpes simplex virus proteins from the trans-golgi network to cell junctions without enveloped capsids.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 74 citations in OpenAlex.
- Article
- The functions of herpesvirus shuttling proteins in the virus lifecycle.Frontiers in microbiology · 2025Review
- The loss of both pUL16 and pUL21 in HSV-1 infected cells abolishes cytoplasmic envelopment.bioRxiv : the preprint server for biology · 2024Article
- Current Insights into the Maturation of Epstein-Barr Virus Particles.Microorganisms · 2024Review
- Glycoengineered keratinocyte library reveals essential functions of specific glycans for all stages of HSV-1 infection.Nature communications · 2023Article
- Mechanism of herpesvirus UL24 protein regulating viral immune escape and virulence.Frontiers in microbiology · 2023Review
- Regulation of alphaherpesvirus protein via post-translational phosphorylation.Veterinary research · 2022Review
- Viral use and subversion of membrane organization and trafficking.Journal of cell science · 2021Review
- HSV-1 Cytoplasmic Envelopment and Egress.International journal of molecular sciences · 2020Review
- Epstein-Barr Virus Exploits the Secretory Pathway to Release Virions.Microorganisms · 2020Article
- Article
- Article
- Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019Review
- The HSV-1 mechanisms of cell-to-cell spread and fusion are critically dependent on host PTP1B.PLoS pathogens · 2018Article
- Epstein-Barr Virus Acquires Its Final Envelope on Intracellular Compartments With Golgi Markers.Frontiers in microbiology · 2018Article
- Experimental Dissection of the Lytic Replication Cycles of Herpes Simplex VirusesFrontiers in microbiology · 2018Review
- Herpes Simplex Virus gE/gI and US9 Promote both Envelopment and Sorting of Virus Particles in the Cytoplasm of Neurons, Two Processes That Precede Anterograde Transport in Axons.Journal of virology · 2017Article
- Cellular Protein WDR11 Interacts with Specific Herpes Simplex Virus Proteins at the trans-Golgi Network To Promote Virus Replication.Journal of virology · 2015Article
- Herpes simplex virus gE/gI extracellular domains promote axonal transport and spread from neurons to epithelial cells.Journal of virology · 2014Article
- Rab6 dependent post-Golgi trafficking of HSV1 envelope proteins to sites of virus envelopment.Traffic (Copenhagen, Denmark) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus (HSV) and other alphaherpesviruses assemble enveloped virions in the trans-Golgi network (TGN) or endosomes. Enveloped particles are formed when capsids bud into TGN/endosomes and virus particles are subsequently ferried to the plasma membrane in TGN-derived vesicles. Little is known about the last stages of virus egress from the TGN/endosomes to cell surfaces except that the HSV directs transport of nascent virions to specific cell surface domains, i.e., epithelial cell junctions. Previously, we showed that HSV glycoprotein gE/gI accumulates extensively in the TGN at early times after infection and also when expressed without other viral proteins. At late times of infection, gE/gI and a cellular membrane protein, TGN46, were redistributed from the TGN to epithelial cell junctions. We show here that gE/gI and a second glycoprotein, gB, TGN46, and another cellular protein, carboxypeptidase D, all moved to cell junctions after infection with an HSV mutant unable to produce cytoplasmic capsids. This redistribution did not involve L particles. In contrast to TGN membrane proteins, several cellular proteins that normally adhere to the cytoplasmic face of TGN, Golgi, and endosomal membranes remained primarily dispersed throughout the cytoplasm. Therefore, cellular and viral membrane TGN proteins move to cell junctions at late times of HSV infection when the production of enveloped particles is blocked. This is consistent with the hypothesis that there are late HSV proteins that reorganize or redistribute TGN/endosomal compartments to promote virus egress and cell-to-cell spread.
Indexed as
Identifiers
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.